Dr. Manuel Mayr, MD, PhD - King's College London - British Heart Foundation Professor of Cardiovascular Proteomics

Dr. Manuel Mayr

MD, PhD

King's College London

British Heart Foundation Professor of Cardiovascular Proteomics

London | United Kingdom

Main Specialties: Biology

Additional Specialties: Biomarkers, Proteomics, Metabolomics, MicroRNAs

ORCID logohttps://orcid.org/0000-0002-0597-829X


Top Author

Dr. Manuel Mayr, MD, PhD - King's College London - British Heart Foundation Professor of Cardiovascular Proteomics

Dr. Manuel Mayr

MD, PhD

Introduction

Manuel Mayr qualified in Medicine from the University of Innsbruck (Austria) in 1999. He then moved to London to undertake a PhD. Upon completion of his PhD, he achieved promotion to Professor in 2011. He has been awarded a prestigious British Heart Foundation Personal Chair in 2017. His academic achievements have been recognised by the inaugural Michael Davies Early Career Award of the British Cardiovascular Society (2007), the inaugural Bernard and Joan Marshall Research Excellence Prize of the British Society for Cardiovascular Research (2010), and the Outstanding Achievement Award by the European Society of Cardiology Council for Basic Cardiovascular Science (2013).

Primary Affiliation: King's College London - London , United Kingdom

Specialties:

Additional Specialties:


View Dr. Manuel Mayr’s Resume / CV

Education

Jul 2001 - May 2005
University of London
PhD
St George's Medical School
Oct 1992 - Jan 1999
Medical University of Innsbruck
MD
Jan 1999
University of Innsbruck
MD
Sub auspiciis Praesidentis

Experience

Sep 2018
Nucleus Member of the ESC Working Group on Myocardial Function
Ex-officio member
Sep 2018
Congress Programme Committee of the ESC
Member
Sep 2017
Proteomics Core at KCL
Academic Lead
Sep 2017
KCL BHF 4-year MRes PhD course
Prrogramme Director
Sep 2017
British Atherosclerosis Society
President
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2011 - Apr 2017
King's College London
Professor of Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
Sep 2011
Leadership committee of the AHA – FGTB Council
Member
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2010 - Jan 2011
King's College London
Reader
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2008 - Jan 2010
King's College London
Senior Lecturer
British Heart Foundation Centre of Excellence
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
Jan 2006 - Jan 2008
King's College London
Lecturer
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence
May 2017
King's College London
BHF Professor for Cardiovascular Proteomics
British Heart Foundation Centre of Excellence

Publications

255Publications

2415Reads

1186Profile Views

3432PubMed Central Citations

Expanding the horizons of microRNA bioinformatics.

RNA 2018 08 5;24(8):1005-1017. Epub 2018 Jun 5.

Institute of Cardiovascular Science, University College London, London WC1E 6JF, United Kingdom.

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http://dx.doi.org/10.1261/rna.065565.118DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6049505PMC
August 2018
8 Reads
4.940 Impact Factor

Non-coding RNAs in vascular disease - from basic science to clinical applications: scientific update from the Working Group of Myocardial Function of the European Society of Cardiology.

Cardiovasc Res 2018 Aug;114(10):1281-1286

Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str.1, 30625 Hannover, Germany.

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http://dx.doi.org/10.1093/cvr/cvy121DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6054241PMC
August 2018
14 Reads
5.940 Impact Factor

Proteomics of the epicardial fat secretome and its role in post-operative atrial fibrillation.

Europace 2018 07;20(7):1201-1208

Department of Cardiothoracic Surgery, St. George's Hospital, University of London, Blackshaw Road, London, UK.

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http://dx.doi.org/10.1093/europace/eux113DOI Listing
July 2018
28 Reads
3.050 Impact Factor

Role of ADAMTS-5 in Aortic Dilatation and Extracellular Matrix Remodeling.

Arterioscler Thromb Vasc Biol 2018 Jul 5;38(7):1537-1548. Epub 2018 Apr 5.

From the King's British Heart Foundation Centre, King's College London, United Kingdom (M.F., J.B.-B., U.M., R.L., A.D., F.B., M.L., N.C., A.J., T.B., X.Y., M.M.)

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http://dx.doi.org/10.1161/ATVBAHA.117.310562DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6026471PMC
July 2018
34 Reads
2 Citations
6.000 Impact Factor

MicroRNA-24 and the Diabetic Heart.

JACC Basic Transl Sci 2018 Jun 25;3(3):363-365. Epub 2018 Jun 25.

King's British Heart Foundation Centre, King's College London, London, United Kingdom.

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http://dx.doi.org/10.1016/j.jacbts.2018.05.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6059003PMC
June 2018
3 Reads

Extracellular Vesicle Crosstalk Between the Myocardium and Immune System Upon Infarction.

Circ Res 2018 Jun;123(1):15-17

From the King's British Heart Foundation Centre, King's College London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.118.313179DOI Listing
June 2018
3 Reads
11.020 Impact Factor

MicroRNA-21 and the Vulnerability of Atherosclerotic Plaques.

Mol Ther 2018 04 21;26(4):938-940. Epub 2018 Mar 21.

King's British Heart Foundation Centre, King's College London, London, UK. Electronic address:

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http://dx.doi.org/10.1016/j.ymthe.2018.03.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6080134PMC
April 2018
6 Reads
1 Citation
6.230 Impact Factor

Cardiac myocyte β3-adrenergic receptors prevent myocardial fibrosis by modulating oxidant stress-dependent paracrine signaling.

Eur Heart J 2018 Mar;39(10):888-898

Department of Medicine, Pole of Pharmacology and Therapeutics (FATH), Institut de Recherche Expérimentale et Clinique (IREC), Cliniques Universitaires Saint-Luc, Université catholique de Louvain, 52 avenue Mounier, 1200 Brussels, Belgium.

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http://dx.doi.org/10.1093/eurheartj/ehx366DOI Listing
March 2018
23 Reads
3 Citations
15.203 Impact Factor

High-density lipoproteins in high resolution: Will proteomics solve the paradox for cardiovascular risk?

Proteomics 2017 02;17(3-4)

King's British Heart Foundation Centre, King's College London, London, UK.

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http://dx.doi.org/10.1002/pmic.201600426DOI Listing
February 2017
9 Reads
3.810 Impact Factor

Diabetes Mellitus-Induced Microvascular Destabilization in the Myocardium.

J Am Coll Cardiol 2017 Jan;69(2):131-143

I. Medizinische Klinik und Poliklinik, University Clinic Rechts der Isar, Technical University of Munich, Munich, Germany; DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany; Walter-Brendel-Centre for Experimental Medicine, Ludwig Maximilian University of Munich, Munich, Germany. Electronic address:

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http://dx.doi.org/10.1016/j.jacc.2016.10.058DOI Listing
January 2017
41 Reads
8 Citations
16.503 Impact Factor

Premature senescence of endothelial cells upon chronic exposure to TNFα can be prevented by N-acetyl cysteine and plumericin.

Sci Rep 2017 01 3;7:39501. Epub 2017 Jan 3.

Department of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, 1090 Vienna, Austria.

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http://dx.doi.org/10.1038/srep39501DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5206708PMC
January 2017
18 Reads
11 Citations
5.080 Impact Factor

MicroRNAs in Cardiovascular Disease.

J Am Coll Cardiol 2016 Dec;68(23):2577-2584

King's British Heart Foundation Centre, King's College London, London, United Kingdom. Electronic address:

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http://dx.doi.org/10.1016/j.jacc.2016.09.945DOI Listing
December 2016
7 Reads
33 Citations
16.503 Impact Factor

Systems biology-opportunities and challenges: the application of proteomics to study the cardiovascular extracellular matrix.

Cardiovasc Res 2016 12 15;112(3):626-636. Epub 2016 Sep 15.

King's British Heart Foundation Centre, King's College London, 125 Coldharbour Lane, London SE5 9NU, UK

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http://dx.doi.org/10.1093/cvr/cvw206DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5157133PMC
December 2016
8 Reads
4 Citations
5.940 Impact Factor

Potential and Caveats of Lipidomics for Cardiovascular Disease.

Circulation 2016 11 18;134(21):1651-1654. Epub 2016 Oct 18.

From Department of Neurology, Medical University of Innsbruck, Austria (R.P., S.K.); and King's British Heart Foundation Centre, King's College London, United Kingdom (M.M.).

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http://dx.doi.org/10.1161/CIRCULATIONAHA.116.025092DOI Listing
November 2016
7 Reads
2 Citations
14.430 Impact Factor

Liver microRNAs: potential mediators and biomarkers for metabolic and cardiovascular disease?

Eur Heart J 2016 Nov 20;37(43):3260-3266. Epub 2016 Apr 20.

King's British Heart Foundation Centre, King's College London, London, UK

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http://dx.doi.org/10.1093/eurheartj/ehw146DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5146692PMC
November 2016
18 Reads
19 Citations
15.203 Impact Factor

Caveats of Untargeted Metabolomics for Biomarker Discovery.

J Am Coll Cardiol 2016 09;68(12):1294-6

King's British Heart Foundation Centre, King's College London, United Kingdom. Electronic address:

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http://dx.doi.org/10.1016/j.jacc.2016.05.098DOI Listing
September 2016
5 Reads
3 Citations
16.503 Impact Factor

Glycoproteomics Reveals Decorin Peptides With Anti-Myostatin Activity in Human Atrial Fibrillation.

Circulation 2016 Sep 24;134(11):817-32. Epub 2016 Aug 24.

From King's British Heart Foundation Centre, King's College London, United Kingdom (J.B.-B., A. Zoccarato, R.K.-T., M.F., X.Y., A. Zampetaki, M.C., P.W., A.M.S., K.O., M.M.); Institute for Molecular and Translational Therapeutic Strategies, MH-Hannover, Germany (S.K.G., T.T.); St George's Hospital, NHS Trust, London, United Kingdom (M.F., A.V., A.K., M.J.); University Medical Center Hamburg-Eppendorf, Germany (T.W., M.N.H.); Protein Metrics, San Carlos, CA (M.B.); Biobanco A Coruña, INIBIC-Complexo Hospitalario Universitario de A Coruña, Spain (N.D.); Institut für Allgemeine Pharmakologie und Toxikologie, Klinikum der Goethe-Universität Frankfurt, Frankfurt am Main, Germany (L.S.); Institute for Pharmacology and Clinical Pharmacology, Heinrich-Heine-University, Düsseldorf, Germany (J.W.F.); Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA (R.V.I.); Thermo Fisher Scientific, San Jose, CA (R.V.); Experimental Cardiology, Department of Cardiology and Angiology, MH-Hannover, Germany (J.H.); and Laboratoire Vecteurs: Synthèse et Applications Thérapeutiques, UMR 7199 CNRS Université de Strasbourg, Illkirch, France (A.K.).

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5081096PMC
http://dx.doi.org/10.1161/CIRCULATIONAHA.115.016423DOI Listing
September 2016
34 Reads
7 Citations
14.430 Impact Factor

Proteomic and metabolomic changes driven by elevating myocardial creatine suggest novel metabolic feedback mechanisms.

Amino Acids 2016 08 3;48(8):1969-81. Epub 2016 May 3.

Division of Cardiovascular Medicine, Radcliffe Department of Medicine, and the BHF Centre of Research Excellence, University of Oxford, Oxford, UK.

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http://dx.doi.org/10.1007/s00726-016-2236-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4974297PMC
August 2016
13 Reads
4 Citations
3.293 Impact Factor

Identification of cyclins A1, E1 and vimentin as downstream targets of heme oxygenase-1 in vascular endothelial growth factor-mediated angiogenesis.

Sci Rep 2016 07 8;6:29417. Epub 2016 Jul 8.

Vascular Sciences, Imperial Centre for Translational and Experimental Medicine, National Heart and Lung Institute, Imperial College London, Hammersmith Hospital, London, UK.

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http://dx.doi.org/10.1038/srep29417DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4937390PMC
July 2016
28 Reads
2 Citations
5.080 Impact Factor

Chronic miR-29 antagonism promotes favorable plaque remodeling in atherosclerotic mice.

EMBO Mol Med 2016 06 1;8(6):643-53. Epub 2016 Jun 1.

Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Department of Pharmacology, School of Medicine Yale University, New Haven, CT, USA

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http://dx.doi.org/10.15252/emmm.201506031DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888854PMC
June 2016
16 Reads
11 Citations
8.665 Impact Factor

Extracellular matrix remodelling in response to venous hypertension: proteomics of human varicose veins.

Cardiovasc Res 2016 06 11;110(3):419-30. Epub 2016 Apr 11.

King's British Heart Foundation Centre, King's College London, 125 Coldharbour Lane, London SE5 9NU, UK

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http://dx.doi.org/10.1093/cvr/cvw075DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872879PMC
June 2016
8 Reads
5 Citations
5.940 Impact Factor

Functional Genomics of Cardioprotection by Ischemic Conditioning and the Influence of Comorbid Conditions: Implications in Target Identification.

Curr Drug Targets 2015 ;16(8):904-11

Department of Pharmacology and Pharmacotherapy, Semmelweis University, Nagyvarad ter 4, Budapest, H-1089, Hungary.

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May 2016
14 Reads
12 Citations
3.021 Impact Factor

Loss of Biglycan Enhances Thrombin Generation in Apolipoprotein E-Deficient Mice: Implications for Inflammation and Atherosclerosis.

Arterioscler Thromb Vasc Biol 2016 05 31;36(5):e41-50. Epub 2016 Mar 31.

From the Institut für Pharmakologie und Klinische Pharmakologie, Universitätsklinikum der Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany (M.G., C.K., A.M.-B., K.F., S.H., J.M., L.-S.K., F.S., N.N., J.W.F.); Cardiovascular Research Institute Düsseldorf (CARID), Universitätsklinikum der Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany (M.G., C.K., A.M.-B., K.F., S.H., J.M., L.-S.K., F.S., N.N., A.P., J.W.F.); Klinik für Kardiologie, Pneumologie und Angiologie, Universitätsklinikum der Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany (A.P.); Pharmazentrum Frankfurt, Institut für Allgemeine Pharmakologie und Toxikologie/ZAFES, Klinikum der Goethe-Universität, Frankfurt am Main, Germany (J.Z.-B., L.S.); Institut für Hämostaseologie, Hämotherapie und Transfusionsmedizin, Universitätsklinikum der Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany (N.S.G., M.E.); King's British Heart Foundation Centre, King's College London, London, United Kingdom (P.S., X.Y., M.M.); and Division of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington (L.R.T.).

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http://atvb.ahajournals.org/content/early/2016/03/31/ATVBAHA
Web Search
http://atvb.ahajournals.org/lookup/doi/10.1161/ATVBAHA.115.3
Publisher Site
http://dx.doi.org/10.1161/ATVBAHA.115.306973DOI Listing
May 2016
28 Reads
6 Citations
6.000 Impact Factor

Guidelines for the functional annotation of microRNAs using the Gene Ontology.

RNA 2016 May 25;22(5):667-76. Epub 2016 Feb 25.

Centre for Cardiovascular Genetics, Institute of Cardiovascular Science, University College London, London WC1E 6JF, United Kingdom.

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http://dx.doi.org/10.1261/rna.055301.115DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4836642PMC
May 2016
13 Reads
7 Citations
4.940 Impact Factor

Oxidant-induced Interprotein Disulfide Formation in Cardiac Protein DJ-1 Occurs via an Interaction with Peroxiredoxin 2.

J Biol Chem 2016 May 4;291(19):10399-410. Epub 2016 Mar 4.

From the King's College London, Cardiovascular Division, The British Heart Foundation Centre of Excellence, The Rayne Institute, St. Thomas' Hospital, London SE1 7EH, United Kingdom and

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http://dx.doi.org/10.1074/jbc.M115.699850DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4858985PMC
May 2016
8 Reads
2 Citations
4.573 Impact Factor

Pharmacogenetics of Clopidogrel: An Unresolved Issue.

Circ Cardiovasc Genet 2016 Apr;9(2):185-8

From the Divisions of Cardiovascular Diseases (N.L.P., J.B.G., C.S.R.), Molecular Pharmacology and Experimental Therapeutics (N.L.P.), Mayo Clinic, Rochester, MN; Cardiovascular Division, King's British Heart Foundation Centre, King's College London, London, United Kingdom (M.M.); and Department of Medicine, Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC (S.H.S.).

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http://dx.doi.org/10.1161/CIRCGENETICS.115.001318DOI Listing
April 2016
11 Reads
2 Citations
5.340 Impact Factor

"Young at heart": Regenerative potential linked to immature cardiac phenotypes.

J Mol Cell Cardiol 2016 Mar 28;92:105-8. Epub 2016 Jan 28.

King's British Heart Foundation Centre, King's College London, London, UK. Electronic address:

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http://dx.doi.org/10.1016/j.yjmcc.2016.01.026DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4796039PMC
March 2016
9 Reads
2 Citations
4.660 Impact Factor

Vascular proteomics in metabolic and cardiovascular diseases

Journal of Internal Medicine

The vasculature is essential for proper organ function. Many pathologies are directly and indirectly related to vascular dysfunction, which causes significant morbidity and mortality. A common pathophysiological feature of diseased vessels is extracellular matrix (ECM) remodelling. Analysing the protein composition of the ECM by conventional antibody-based techniques is challenging; alternative splicing or post-translational modifications, such as glycosylation, can mask epitopes required for antibody recognition. By contrast, proteomic analysis by mass spectrometry enables the study of proteins without the constraints of antibodies. Recent advances in proteomic techniques make it feasible to characterize the composition of the vascular ECM and its remodelling in disease. These developments may lead to the discovery of novel prognostic and diagnostic markers. Thus, proteomics holds potential for identifying ECM signatures to monitor vascular disease processes. Furthermore, a better understanding of the ECM remodelling processes in the vasculature might make ECM-associated proteins more attractive targets for drug discovery efforts. In this review, we will summarize the role of the ECM in the vasculature. Then, we will describe the challenges associated with studying the intricate network of ECM proteins and the current proteomic strategies to analyse the vascular ECM in metabolic and cardiovascular diseases.

https://kclpure.kcl.ac.uk/portal/en/publications/vascular-proteomics-in-metabolic-and-cardiovascular-diseases(f3c342a1-c486-43b9-b97d-c37e952c2402).html

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March 2016
2 Reads

"Young at heart"

Journal of Molecular and Cellular Cardiology

The adult human myocardium is incapable of regeneration; yet, the zebrafish (Danio rerio) can regenerate damaged myocardium. Similar to the zebrafish heart, hearts of neonatal, but not adult mice are capable of myocardial regeneration. We performed a proteomics analysis of adult zebrafish hearts and compared their protein expression profile to hearts from neonatal and adult mice. Using difference in-gel electrophoresis (DIGE), there was little overlap between the proteome from adult mouse (>. 8 weeks old) and adult zebrafish (18 months old) hearts. Similarly, there was a significant degree of mismatch between the protein expression in neonatal and adult mouse hearts. Enrichment analysis of the selected proteins revealed over-expression of DNA synthesis-related proteins in the cardiac proteome of the adult zebrafish heart similar to neonatal and 4 days old mice, whereas in hearts of adult mice there was a mitochondria-related predominance in protein expression. Importantly, we noted pronounced differences in the myofilament composition: the adult zebrafish heart lacks many of the myofilament proteins of differentiated adult cardiomyocytes such as the ventricular isoforms of myosin light chains and nebulette. Instead, troponin I and myozenin 1 were expressed as skeletal isoforms rather than cardiac isoforms. The relative immaturity of the adult zebrafish heart was further supported by cardiac microRNA data. Our assessment of zebrafish and mammalian hearts challenges the assertions on the translational potential of cardiac regeneration in the zebrafish model. The immature myofilament composition of the fish heart may explain why adult mouse and human cardiomyocytes lack this endogenous repair mechanism.

https://kclpure.kcl.ac.uk/portal/en/publications/young-at-heart(967bc1cc-b8b4-4126-a40f-0054c7b2a594).html

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March 2016
4 Reads

Inadequate hepcidin serum concentrations predict incident type 2 diabetes mellitus.

Diabetes Metab Res Rev 2016 Feb 29;32(2):187-92. Epub 2015 Oct 29.

Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.

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http://dx.doi.org/10.1002/dmrr.2711DOI Listing
February 2016
15 Reads
4 Citations

When Sweet Turns Salty: Glucose-Induced Suppression of Atrial Natriuretic Peptide by MicroRNA-425.

J Am Coll Cardiol 2016 Feb;67(7):813-6

King's British Heart Foundation Centre, King's College London, London, United Kingdom. Electronic address:

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http://dx.doi.org/10.1016/j.jacc.2015.12.008DOI Listing
February 2016
6 Reads
1 Citation
16.503 Impact Factor

Angiogenic microRNAs Linked to Incidence and Progression of Diabetic Retinopathy in Type 1 Diabetes.

Diabetes 2016 Jan 22;65(1):216-27. Epub 2015 Sep 22.

King's British Heart Foundation Centre of Research Excellence, King's College London, London, U.K.

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http://dx.doi.org/10.2337/db15-0389DOI Listing
January 2016
14 Reads
13 Citations
8.100 Impact Factor

MicroRNA Biomarkers for Coronary Artery Disease?

Curr Atheroscler Rep 2015 Dec;17(12):70

King's British Heart Foundation Centre, King's College London, 125 Coldharbour Lane, London, SE59NU, UK.

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http://dx.doi.org/10.1007/s11883-015-0548-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4613887PMC
December 2015
41 Reads
6 Citations
3.420 Impact Factor

Comparative analysis of statistical methods used for detecting differential expression in label-free mass spectrometry proteomics.

J Proteomics 2015 Nov 18;129:83-92. Epub 2015 Jul 18.

King's British Heart Foundation Centre, King's College London, London, UK.

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http://dx.doi.org/10.1016/j.jprot.2015.07.012DOI Listing
November 2015
10 Reads
9 Citations
3.890 Impact Factor

Novel methodologies for biomarker discovery in atherosclerosis.

Eur Heart J 2015 Oct 5;36(39):2635-42. Epub 2015 Jun 5.

Ludwig-Maximilians-University, G02.523, Heidelberglaan 100, 3584CX Munich, Germany German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.

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http://eurheartj.oxfordjournals.org/content/ehj/36/39/2635.f
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http://eurheartj.oxfordjournals.org/lookup/doi/10.1093/eurhe
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http://dx.doi.org/10.1093/eurheartj/ehv236DOI Listing
October 2015
20 Reads
22 Citations
15.203 Impact Factor

XBP 1-Deficiency Abrogates Neointimal Lesion of Injured Vessels Via Cross Talk With the PDGF Signaling.

Arterioscler Thromb Vasc Biol 2015 Oct 27;35(10):2134-44. Epub 2015 Aug 27.

From the Cardiovascular Division, King's College London BHF Centre, London, United Kingdom (L.Z., Y.L., J.Y., A.Z., X.Y., M.M., Y.H., Q.X.); Institute of Bioengineering (J.Y., W.W.) and Centre for Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry (Q.X.), Queen Mary University of London, London, United Kingdom; Department of Emergency Medicine, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China (G.W.); Centre for Experimental Medicine, Queen's University Belfast, Belfast, United Kingdom (A.M.); and Department of Biophysics, Graduate School of Science, Kyoto University, Kyoto, Japan (K.M.).

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http://atvb.ahajournals.org/lookup/doi/10.1161/ATVBAHA.115.3
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http://dx.doi.org/10.1161/ATVBAHA.115.305420DOI Listing
October 2015
13 Reads
6 Citations
6.000 Impact Factor

Sweet dicer: impairment of micro-RNA processing by diabetes.

Circ Res 2015 Jul;117(2):116-8

From the Cardiovascular Division, King's British Heart Foundation Centre, King's College London, London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.117.306817DOI Listing
July 2015
13 Reads
2 Citations
11.020 Impact Factor

Asymmetric dimethylarginine and cardiovascular risk: systematic review and meta-analysis of 22 prospective studies.

J Am Heart Assoc 2015 May 28;4(6):e001833. Epub 2015 May 28.

Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, United Kingdom (P.W., D.F.F., R.G., E.D.A., R.C.).

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http://dx.doi.org/10.1161/JAHA.115.001833DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4599532PMC
May 2015
26 Reads
26 Citations
2.882 Impact Factor

Proteomic analyses reveal that loss of TDP-43 affects RNA processing and intracellular transport

Neuroscience

Transactive response DNA-binding protein 43 (TDP-43) is a predominantly nuclear, ubiquitously expressed RNA and DNA-binding protein. It recognizes and binds to UG repeats and is involved in pre-mRNA splicing, mRNA stability and microRNA metabolism. TDP-43 is essential in early embryonic development but accumulates in cytoplasmic aggregates in amyotrophic lateral sclerosis (ALS) and tau-negative frontotemporal lobar degeneration (FTLD). It is not known yet whether cytoplasmic aggregates of TDP-43 are toxic or protective but they are often associated with a loss of TDP-43 from the nucleus and neurodegeneration may be caused by a loss of normal TDP-43 function or a gain of toxic function. Here we present a proteomic study to analyze the effect of loss of TDP-43 on the proteome. MS data are available via ProteomeXchange with identifier PXD001668. Our results indicate that TDP-43 is an important regulator of RNA metabolism and intracellular transport. We show that Ran-binding protein 1 (RanBP1), DNA methyltransferase 3 alpha (Dnmt3a) and chromogranin B (CgB) are downregulated upon TDP-43 knockdown. Subsequently, transportin 1 level is increased as a result of RanBP1 depletion. Improper regulation of these proteins and the subsequent disruption of cellular processes may play a role in the pathogenesis of the TDP-43 proteinopathies ALS and FTLD.

https://kclpure.kcl.ac.uk/portal/en/publications/proteomic-analyses-reveal-that-loss-of-tdp43-affects-rna-processing-and-intracellular-transport(07f3f434-520e-40c5-8f62-48f130ae1e42).html

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May 2015
2 Reads

Vascular smooth muscle cell calcification is mediated by regulated exosome secretion.

Circ Res 2015 Apr 23;116(8):1312-23. Epub 2015 Feb 23.

From the British Heart Foundation Centre of Excellence, Cardiovascular Division, King's College London, The James Black Centre, London, United Kingdom (A.N.K., I.D., D.S., M.F., P.S., D.A.-H., X.Y., M.M., C.M.S.); Department of Biochemistry-Vascular Aspects, Faculty of Medicine, Health and Life Science, Maastricht University, Maastricht, The Netherlands (M.L.L.C., C.P.R., L.J.S.); Hatter Cardiovascular Institute, University College London, London, United Kingdom (Y.Z., S.M.D.); Department of Imaging, King's College London, London, United Kingdom (R.T.M.D.R.); Great Ormond Street Hospital, London, United Kingdom (R.S.); Department of Anatomy, Multi-Imaging Centre, Cambridge, United Kingdom (K.M., J.N.S.); Heart Science Centre, Harefield, United Kingdom (A.C.); and Department of Materials, Imperial College London, London, United Kingdom (S.B.).

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http://circres.ahajournals.org/cgi/doi/10.1161/CIRCRESAHA.11
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http://dx.doi.org/10.1161/CIRCRESAHA.116.305012DOI Listing
April 2015
51 Reads
66 Citations
11.020 Impact Factor

ADAMTS-7 inhibits re-endothelialization of injured arteries and promotes vascular remodeling through cleavage of thrombospondin-1.

Circulation 2015 Mar 20;131(13):1191-201. Epub 2015 Feb 20.

From Deutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen, Technische Universität München, Germany (T.K., H.S.); Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China (L.Z., Z.L.,Y.H.,Y.W., Y.F., X.W., W.K.); Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China (L.Z., Z.L., Y.H., Y.W., Y.F., X.W., W.K.); Cardiovascular Division, Kings College London BHF Centre, United Kingdom (X.Y., M.M., Q.X.); Department of Immunology, School of Basic Medical Sciences, Peking University, Beijing, China (Q.G.); School of Basic Medical Sciences, Tianjin University, Beijing, China (Y.Z.); Institut für Physiologie, Universität zu Lübeck, Germany (K.S., C.d.W.); Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK) e.V. (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, Lübeck, Germany (K.S., C.d.W., J.E., Z.A.); Institut für Integrative und Experimentelle Genomik, Universität zu Lübeck, Germany (J.E., Z.A.); and Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK) e.V. (German Center for Cardiovascular Research), partner site Munich Heart Alliance (MHA), München, Germany (H.S.).

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http://dx.doi.org/10.1161/CIRCULATIONAHA.114.014072DOI Listing
March 2015
23 Reads
14 Citations
14.430 Impact Factor

Cardiac-targeted NADPH oxidase 4 in the adaptive cardiac remodelling of the murine heart.

Lancet 2015 Feb;385 Suppl 1:S73

Cardiovascular Division, King's College London, London, UK.

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http://dx.doi.org/10.1016/S0140-6736(15)60388-9DOI Listing
February 2015
24 Reads
3 Citations
45.220 Impact Factor

The cardiovascular gene annotation initiative: Impact on data analysis

Lovering RC, Rodriguez-Lopez M, Campbell NH, Huntley RP, Sawford T, O’Donovan C, Orchard S, Hermjakob H, Martin M, Mayr M, Humphries SE, Talmud PJ, Atherosclerosis, 2015, vol. 241, no. 1, pp. e37, 2015

http://europepmc.org/abstract/CTX/c7535

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January 2015
1 Read

Affinity proteomics for phosphatase interactions in atrial fibrillation.

J Am Coll Cardiol 2015 Jan;65(2):174-6

King's British Heart Foundation Centre, King's College London, London, United Kingdom. Electronic address:

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http://dx.doi.org/10.1016/j.jacc.2014.11.005DOI Listing
January 2015
4 Reads
16.503 Impact Factor

Native T1 in discrimination of acute and convalescent stages in patients with clinical diagnosis of myocarditis: a proposed diagnostic algorithm using CMR.

JACC Cardiovasc Imaging 2015 Jan 10;8(1):37-46. Epub 2014 Dec 10.

Cardiovascular Imaging Department, Division of Imaging Sciences, King's College London, London, United Kingdom. Electronic address:

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http://dx.doi.org/10.1016/j.jcmg.2014.07.016DOI Listing
January 2015
18 Reads
25 Citations

Lipidomics: quest for molecular lipid biomarkers in cardiovascular disease.

Circ Cardiovasc Genet 2014 Dec;7(6):941-54

From the King's British Heart Foundation Centre, King's College, London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCGENETICS.114.000550DOI Listing
December 2014
7 Reads
15 Citations
5.340 Impact Factor

LDL-receptor-deficient mice lacking microRNA-143/145 have less atherosclerosis.

Thromb Haemost 2014 Oct 11;112(4):629. Epub 2014 Sep 11.

Manuel Mayr, King's British Heart Foundation Centre, King's College London, London, UK, E-mail:

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http://dx.doi.org/10.1160/TH14-09-0734DOI Listing
October 2014
7 Reads
4.984 Impact Factor

Role of miR-195 in aortic aneurysmal disease.

Circ Res 2014 Oct 8;115(10):857-66. Epub 2014 Sep 8.

From the King's British Heart Foundation Centre (A.Z., R.A., U.M., R.S.M.G., A.P., X.Y., S.R.L., R.L., B.F., M.F., J.B.-B., C.M., A.A., M.W., R.B., A.S., M.M.) and Institute of Psychiatry (P.-W.S.), King's College London, United Kingdom; Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom (P.W.); and Department of Cardiac Surgery, St George's Healthcare NHS Trust, London, United Kingdom (M.F., M.J.).

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http://dx.doi.org/10.1161/CIRCRESAHA.115.304361DOI Listing
October 2014
25 Reads
25 Citations
11.020 Impact Factor

Redox state of pentraxin 3 as a novel biomarker for resolution of inflammation and survival in sepsis.

Mol Cell Proteomics 2014 Oct 23;13(10):2545-57. Epub 2014 Jun 23.

From the ‡King's British Heart Foundation Centre, King's College London, SE5 9NU London, UK;

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http://dx.doi.org/10.1074/mcp.M114.039446DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4188985PMC
October 2014
15 Reads
9 Citations
6.564 Impact Factor

Long-term therapeutic silencing of miR-33 increases circulating triglyceride levels and hepatic lipid accumulation in mice.

EMBO Mol Med 2014 Sep;6(9):1133-41

Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Integrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine Yale University School of Medicine, New Haven, CT, USA Leon H. Charney Division of Cardiology, Department of Medicine, New York University School of Medicine, New York, NY, USA Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine, New York, NY, USA

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http://dx.doi.org/10.15252/emmm.201404046DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4197861PMC
September 2014
7 Reads
41 Citations
8.665 Impact Factor

"Going long": long non-coding RNAs as biomarkers.

Circ Res 2014 Sep;115(7):607-9

From the Cardiovascular Division, King's British Heart Foundation Centre, King's College London, London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.114.304839DOI Listing
September 2014
8 Reads
7 Citations
11.020 Impact Factor

Discrimination and net reclassification of cardiovascular risk with lipoprotein(a): prospective 15-year outcomes in the Bruneck Study.

J Am Coll Cardiol 2014 Sep;64(9):851-60

Department of Medicine, University of California San Diego, La Jolla, California. Electronic address:

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http://dx.doi.org/10.1016/j.jacc.2014.03.061DOI Listing
September 2014
27 Reads
28 Citations
16.503 Impact Factor

ESC Working Group on Myocardial Function Position Paper: how to study the right ventricle in experimental models.

Eur J Heart Fail 2014 May 23;16(5):509-18. Epub 2014 Feb 23.

Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Al. Prof. Hernani Monteiro, 4200 319, Porto, Portugal.

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http://dx.doi.org/10.1002/ejhf.66DOI Listing
May 2014
33 Reads
3 Citations
6.530 Impact Factor

Lipidomics profiling and risk of cardiovascular disease in the prospective population-based Bruneck study.

Circulation 2014 May 12;129(18):1821-31. Epub 2014 Mar 12.

King's British Heart Foundation Centre (C.S., S.R.L., U.M., M. Mayr) and Department of Twin Research & Genetic Epidemiology (M. Mangino, C.M., A.M., T.D.R.), King's College London, London, UK; Department of Neurology, Medical University Innsbruck, Innsbruck, Austria (R.P., P.W., J.W., S.K.); Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK (P.W.); and Departments of Laboratory Medicine and Neurology, Bruneck Hospital, Bruneck, Italy (P.S., G.R.).

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http://dx.doi.org/10.1161/CIRCULATIONAHA.113.002500DOI Listing
May 2014
17 Reads
58 Citations
14.430 Impact Factor

Tracing the proteomic fingerprint of the diabetic aorta?

Circ Cardiovasc Genet 2014 Apr;7(2):100-1

King's British Heart Foundation Centre, King's College London, London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCGENETICS.114.000592DOI Listing
April 2014
7 Reads
5.340 Impact Factor

Effects of heparin on temporal microRNA profiles.

J Am Coll Cardiol 2014 Mar 4;63(9):940-1. Epub 2013 Dec 4.

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http://dx.doi.org/10.1016/j.jacc.2013.07.118DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5357045PMC
March 2014
8 Reads
5 Citations
16.503 Impact Factor

Matrix metalloproteinase-8 promotes vascular smooth muscle cell proliferation and neointima formation.

Arterioscler Thromb Vasc Biol 2014 Jan 24;34(1):90-8. Epub 2013 Oct 24.

From William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom (Q. Xiao, F.Z., S.Y.); Department of Cardiology, Peking University People's Hospital, Beijing, China (F.Z.); Department of Pharmacy, University of Naples Federico II, Naples, Italy (G.G., M. Maddaluno, P.M., A.I.); Cardiovascular Division, King's College London BHF Centre, London, United Kingdom (Y.H., Z.Z., Q. Xing, X.Y., M. Mayr, Q. Xu); Clemens Schöpf Institute, Technische Universität Darmstadt, Darmstadt, Germany (B.D., B.S.); Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom (P.M.).

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http://atvb.ahajournals.org/cgi/doi/10.1161/ATVBAHA.113.3014
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http://dx.doi.org/10.1161/ATVBAHA.113.301418DOI Listing
January 2014
13 Reads
13 Citations
6.000 Impact Factor

Phosphoregulation of the titin-cap protein telethonin in cardiac myocytes.

J Biol Chem 2014 Jan 26;289(3):1282-93. Epub 2013 Nov 26.

From the Cardiovascular Division, King's College London British Heart Foundation Centre, London SE1 7EH, United Kingdom.

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http://dx.doi.org/10.1074/jbc.M113.479030DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3894314PMC
January 2014
26 Reads
10 Citations
4.573 Impact Factor

Gestational diabetes mellitus impairs Nrf2-mediated adaptive antioxidant defenses and redox signaling in fetal endothelial cells in utero.

Diabetes 2013 Dec 23;62(12):4088-97. Epub 2013 Aug 23.

Cardiovascular Division, British Heart Foundation Centre of Research Excellence, King's College London, London, U.K.

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http://dx.doi.org/10.2337/db13-0169DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3837032PMC
December 2013
11 Reads
24 Citations
8.100 Impact Factor

Gene network and proteomic analyses of cardiac responses to pathological and physiological stress.

Circ Cardiovasc Genet 2013 Dec 8;6(6):588-97. Epub 2013 Nov 8.

Cardiovascular Division, King's College London BHF Centre of Research Excellence, School of Medicine, James Black Centre, London, United Kingdom.

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http://circgenetics.ahajournals.org/content/early/2013/11/08
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http://circgenetics.ahajournals.org/cgi/doi/10.1161/CIRCGENE
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http://dx.doi.org/10.1161/CIRCGENETICS.113.000063DOI Listing
December 2013
16 Reads
7 Citations
5.340 Impact Factor

Histone deacetylase 3 unconventional splicing mediates endothelial-to-mesenchymal transition through transforming growth factor β2.

J Biol Chem 2013 Nov 17;288(44):31853-66. Epub 2013 Sep 17.

From the Cardiovascular Division, King's College London BHF Centre, 125 Cold Harbour Lane, London SE5 9NU, United Kingdom.

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http://dx.doi.org/10.1074/jbc.M113.463745DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3814778PMC
November 2013
10 Reads
6 Citations
4.573 Impact Factor

A sequential extraction methodology for cardiac extracellular matrix prior to proteomics analysis.

Methods Mol Biol 2013 ;1005:215-23

King's British Heart Foundation Centre, London, UK.

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http://dx.doi.org/10.1007/978-1-62703-386-2_17DOI Listing
October 2013
7 Reads
13 Citations

Multidimensional separation prior to mass spectrometry: getting closer to the bottom of the iceberg.

Proteomics 2013 Oct;13(20):2942-3

King's British Heart Foundation Centre, King's College London, London, UK.

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http://dx.doi.org/10.1002/pmic.201300400DOI Listing
October 2013
4 Reads
3.810 Impact Factor

Oxidative stress in atherosclerosis: the role of microRNAs in arterial remodeling.

Free Radic Biol Med 2013 Sep 21;64:69-77. Epub 2013 Jun 21.

King's British Heart Foundation Centre, King's College London, London SE5 9NU, UK.

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http://dx.doi.org/10.1016/j.freeradbiomed.2013.06.025DOI Listing
September 2013
7 Reads
14 Citations
5.740 Impact Factor

MicroRNA biomarkers for failing hearts?

Eur Heart J 2013 Sep 25;34(36):2782-3. Epub 2013 Jul 25.

King's British Heart Foundation Centre, King's College London, UK; and.

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http://dx.doi.org/10.1093/eurheartj/eht261DOI Listing
September 2013
8 Reads
3 Citations
15.203 Impact Factor

Oxidative stress in atherosclerosis

Free Radical Biology and Medicine

Atherosclerosis is the underlying condition in most cardiovascular diseases. Among the highly specific cellular and molecular responses, endothelial dysfunction plays a key role in disease initiation and progression. These events coincide with the occurrence of oxidative stress. Increased reactive oxygen species production and oxidization of low-density lipoprotein are detected throughout atherosclerosis progression. MicroRNAs (miRNAs) have emerged as important regulators of gene expression that posttranscriptionally modify cellular responses and function. Accumulating studies indicate an integrated miRNA network in the molecular mechanisms that control cellular homeostasis, vascular inflammation, and metabolism. Experimental models of atherosclerosis highlight a direct link between altered miRNA expression profiles and the pathophysiology of the disease and identify putative miRNA candidates for the development of novel therapeutic strategies. In this review, we provide an overview of the role of miRNA regulatory networks in oxidative stress in atherosclerosis and arterial remodeling and discuss their potential therapeutic implications. 

https://kclpure.kcl.ac.uk/portal/en/publications/oxidative-stress-in-atherosclerosis(c7c50ccf-e78f-477d-b511-a9a875202b2f).html

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September 2013
3 Reads

Impact of intravenous heparin on quantification of circulating microRNAs in patients with coronary artery disease.

Thromb Haemost 2013 Sep 27;110(3):609-15. Epub 2013 Jun 27.

Prof. Manuel Mayr, King's British Heart Foundation Centre, King's College London, London, SE5 9NU, UK, Tel.: +44 02078 485132, Fax: +44 2078485296, E-mail:

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http://www.vascular-proteomics.com/pub/2013/KaudewitzD_Throm
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http://www.schattauer.de/index.php?id=1214&doi=10.1160/T
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http://dx.doi.org/10.1160/TH13-05-0368DOI Listing
September 2013
19 Reads
16 Citations
4.984 Impact Factor

The Hypoxia-Inducible MicroRNA Cluster miR-199a similar to 214 Targets Myocardial PPAR delta and Impairs Mitochondrial Fatty Acid Oxidation

CELL METABOLISM

Peroxisome proliferator-activated receptor δ (PPARδ) is a critical regulator of energy metabolism in the heart. Here, we propose a mechanism that integrates two deleterious characteristics of heart failure, hypoxia and a metabolic shift toward glycolysis, involving the microRNA cluster miR-199a∼214 and PPARδ. We demonstrate that under hemodynamic stress, cardiac hypoxia activates DNM3os, a noncoding transcript that harbors the microRNA cluster miR-199a∼214, which shares PPARδ as common target. To address the significance of miR-199a∼214 induction and concomitant PPARδ repression, we performed antagomir-based silencing of both microRNAs and subjected mice to biomechanical stress to induce heart failure. Remarkably, antagomir-treated animals displayed improved cardiac function and restored mitochondrial fatty acid oxidation. Taken together, our data suggest a mechanism whereby miR-199a∼214 actively represses cardiac PPARδ expression, facilitating a metabolic shift from predominant reliance on fatty acid utilization in the healthy myocardium toward increased reliance on glucose metabolism at the onset of heart failure.

https://kclpure.kcl.ac.uk/portal/en/publications/the-hypoxiainducible-microrna-cluster-mir199a-similar-to-214-targets-myocardial-ppar-delta-and-impairs-mitochondrial-fatty-acid-oxidation(cd752148-75b3-4e7a-8f1b-abf59b0c05a6).html

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September 2013
2 Reads

Vascular proteomics--the forgotten blood vessels.

Authors:
Manuel Mayr

Proteomics Clin Appl 2013 Aug;7(7-8):463

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http://dx.doi.org/10.1002/prca.201370044DOI Listing
August 2013
6 Reads
2.683 Impact Factor

Proteomics in aortic aneurysm--what have we learnt so far?

Proteomics Clin Appl 2013 Aug 9;7(7-8):504-15. Epub 2013 Jul 9.

Department of Cardiothoracic Surgery, St George's Hospital University of London, London, UK.

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http://dx.doi.org/10.1002/prca.201300016DOI Listing
August 2013
6 Reads
4 Citations
2.683 Impact Factor

Proteomics and metabolomics for mechanistic insights and biomarker discovery in cardiovascular disease.

Rev Esp Cardiol (Engl Ed) 2013 Aug 2;66(8):657-61. Epub 2013 Jul 2.

King's British Heart Foundation Centre, King's College of London, London, United Kingdom. Electronic address:

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http://dx.doi.org/10.1016/j.rec.2013.04.009DOI Listing
August 2013
39 Reads
7 Citations

Heterogeneity in neutrophil microparticles reveals distinct proteome and functional properties.

Mol Cell Proteomics 2013 Aug 8;12(8):2205-19. Epub 2013 May 8.

The William Harvey Research Institute, Barts and The London School of Medical, Charterhouse Square, London EC1M 6BQ, United Kingdom.

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http://www.vascular-proteomics.com/pub/2013/DalliJ_MCP_12_22
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http://www.mcponline.org/cgi/doi/10.1074/mcp.M113.028589
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http://dx.doi.org/10.1074/mcp.M113.028589DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3734580PMC
August 2013
16 Reads
36 Citations
6.564 Impact Factor

Proteomics in aortic aneurysm - What have we learnt so far?

Proteomics Clinical Applications

Aortic aneurysm is a deceptively indolent disease that can cause severe complications such as aortic rupture and dissection. In the normal aorta, vascular smooth muscle cells within the medial layer produce and sustain the extracellular matrix (ECM) that provides structural support but also retains soluble growth factors and regulates their distribution. Although the ECM is an obvious target to identify molecular processes leading to structural failure within the vessel wall, an in-depth proteomics analysis of this important sub-proteome has not been performed. Most proteomics analyses of the vasculature to date used homogenized tissue devoid of spatial information. In such homogenates, quantitative proteomics comparisons are hampered by the heterogeneity of clinical samples (i.e. cellular composition) and the dynamic range limitations stemming from highly abundant cellular proteins. An unbiased proteomics discovery approach targeting the ECM instead of the cellular proteome may decipher the complex, multivalent signals that are presented to cells during aortic remodelling. A better understanding of the ECM in healthy and diseased vessels will provide important pathogenic insights and has potential to reveal novel biomarkers. 

https://kclpure.kcl.ac.uk/portal/en/publications/proteomics-in-aortic-aneurysm--what-have-we-learnt-so-far(7a362ea7-0cce-4204-a521-9354788af614).html

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August 2013
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Search Strategies for Glycopeptide Identification.

Becker C, Tang W, Kil YJ, Yin X, Mayr M, Khoo K, Viner R, Bern M, Journal of biomolecular techniques : JBT, 2013, vol. 24, no. Suppl, pp. S33-S33

http://europepmc.org/abstract/PMC/PMC3635383

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May 2013
2 Reads

Endothelial seeding for abdominal aortic aneurysms: lessons learned from the past and present.

Circulation 2013 May 9;127(18):1847-9. Epub 2013 Apr 9.

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http://dx.doi.org/10.1161/CIRCULATIONAHA.113.002573DOI Listing
May 2013
4 Reads
14.430 Impact Factor

Native T1 mapping in differentiation of normal myocardium from diffuse disease in hypertrophic and dilated cardiomyopathy.

JACC Cardiovasc Imaging 2013 Apr 14;6(4):475-84. Epub 2013 Mar 14.

Department of Cardiovascular Imaging, King's College London, London, United Kingdom.

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http://dx.doi.org/10.1016/j.jcmg.2012.08.019DOI Listing
April 2013
4 Reads
72 Citations

Glycoproteomic analysis of the secretome of human endothelial cells.

Mol Cell Proteomics 2013 Apr 23;12(4):956-78. Epub 2013 Jan 23.

The King's British Heart Foundation Centre, King's College London, London SE5 9NU, UK.

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http://dx.doi.org/10.1074/mcp.M112.024018DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617342PMC
April 2013
5 Reads
28 Citations
6.564 Impact Factor

From data gathering to systems medicine.

Authors:
Manuel Mayr

Cardiovasc Res 2013 Mar 5;97(4):599-600. Epub 2013 Feb 5.

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http://dx.doi.org/10.1093/cvr/cvt017DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3583261PMC
March 2013
7 Reads
3 Citations
5.940 Impact Factor

Proteomics: from single molecules to biological pathways.

Cardiovasc Res 2013 Mar 23;97(4):612-22. Epub 2012 Nov 23.

King's British Heart Foundation Centre, King's College London, 125 Coldharbour Lane, London SE5 9NU, UK.

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http://dx.doi.org/10.1093/cvr/cvs346DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3583257PMC
March 2013
5 Reads
13 Citations
5.940 Impact Factor

Proteomic identification of matrix metalloproteinase substrates in the human vasculature.

Circ Cardiovasc Genet 2013 Feb 19;6(1):106-17. Epub 2012 Dec 19.

King's British Heart Foundation Centre, King's College London, London, United Kingdom.

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http://www.vascular-proteomics.com/pub/2012/StegemannC_CircC
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http://circgenetics.ahajournals.org/cgi/doi/10.1161/CIRCGENE
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http://dx.doi.org/10.1161/CIRCGENETICS.112.964452DOI Listing
February 2013
29 Reads
16 Citations
5.340 Impact Factor

MicroRNAs within the continuum of postgenomics biomarker discovery.

Arterioscler Thromb Vasc Biol 2013 Feb;33(2):206-14

King's British Heart Foundation Centre, King's College London, 125 Coldharbour Lane, London SE5 9NU, United Kingdom.

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http://atvb.ahajournals.org/content/33/2/206.full.pdf
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http://atvb.ahajournals.org/cgi/doi/10.1161/ATVBAHA.112.3001
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http://dx.doi.org/10.1161/ATVBAHA.112.300141DOI Listing
February 2013
8 Reads
25 Citations
6.000 Impact Factor

Functional role of matrix metalloproteinase-8 in stem/progenitor cell migration and their recruitment into atherosclerotic lesions.

Circ Res 2013 Jan 15;112(1):35-47. Epub 2012 Oct 15.

William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, John Vane Science Building, Charterhouse Square, London EC1M 6BQ, UK.

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http://circres.ahajournals.org/content/early/2012/10/15/CIRC
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http://circres.ahajournals.org/content/112/1/35.full.pdf
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http://circres.ahajournals.org/cgi/doi/10.1161/CIRCRESAHA.11
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http://dx.doi.org/10.1161/CIRCRESAHA.112.274019DOI Listing
January 2013
9 Reads
13 Citations
11.020 Impact Factor

Cytochrome P4502S1: a novel monocyte/macrophage fatty acid epoxygenase in human atherosclerotic plaques.

Basic Res Cardiol 2013 Jan 7;108(1):319. Epub 2012 Dec 7.

Institute for Vascular Signalling, Centre for Molecular Medicine, Johann Wolfgang Goethe University and DZHK (German Centre for Cardiovascular Research) partner site Rhine-Main, Theodor Stern Kai 7, 60596 Frankfurt am Main, Germany.

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http://dx.doi.org/10.1007/s00395-012-0319-8DOI Listing
January 2013
10 Reads
7 Citations
5.414 Impact Factor

Oxidation-specific biomarkers, prospective 15-year cardiovascular and stroke outcomes, and net reclassification of cardiovascular events.

J Am Coll Cardiol 2012 Nov 1;60(21):2218-29. Epub 2012 Nov 1.

Department of Medicine, University of California San Diego, La Jolla, CA, USA.

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http://dx.doi.org/10.1016/j.jacc.2012.08.979DOI Listing
November 2012
9 Reads
47 Citations
16.503 Impact Factor

Analytical challenges and technical limitations in assessing circulating miRNAs.

Thromb Haemost 2012 Oct 25;108(4):592-8. Epub 2012 May 25.

King's British Heart Foundation Centre, King's College London, London, UK.

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http://dx.doi.org/10.1160/TH12-02-0097DOI Listing
October 2012
4 Reads
29 Citations
4.980 Impact Factor

Calpain inhibition stabilizes the platelet proteome and reactivity in diabetes.

Blood 2012 Jul 4;120(2):415-23. Epub 2012 Jun 4.

Institute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Theodor-Stern-Kai 7, Frankfurt am Main, Germany.

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http://dx.doi.org/10.1182/blood-2011-12-399980DOI Listing
July 2012
13 Reads
7 Citations
10.452 Impact Factor

Prospective study on circulating MicroRNAs and risk of myocardial infarction.

J Am Coll Cardiol 2012 Jul;60(4):290-9

King's British Heart Foundation Centre, King's College London, United Kingdom.

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http://dx.doi.org/10.1016/j.jacc.2012.03.056DOI Listing
July 2012
15 Reads
94 Citations
16.503 Impact Factor

Novel role of ADAMTS-5 protein in proteoglycan turnover and lipoprotein retention in atherosclerosis.

J Biol Chem 2012 Jun 9;287(23):19341-5. Epub 2012 Apr 9.

King's British Heart Foundation Centre, King's College London, London SE5 9NU, United Kingdom.

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http://dx.doi.org/10.1074/jbc.C112.350785DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3365970PMC
June 2012
11 Reads
24 Citations
4.570 Impact Factor

Method for protein subfractionation of cardiovascular tissues before DIGE analysis.

Methods Mol Biol 2012 ;854:287-97

Cardiovascular Division, King's College London, London, UK.

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http://dx.doi.org/10.1007/978-1-61779-573-2_20DOI Listing
May 2012
5 Reads
2 Citations

Profiling of circulating microRNAs: from single biomarkers to re-wired networks.

Cardiovasc Res 2012 Mar 25;93(4):555-62. Epub 2011 Oct 25.

King's British Heart Foundation Centre, King' s College London, 125 Coldharbour Lane, London SE5 9NU, UK.

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http://dx.doi.org/10.1093/cvr/cvr266DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291086PMC
March 2012
7 Reads
55 Citations
5.940 Impact Factor

Profiling of circulating microRNAs

Cardiovascular Research

The recent discovery that microRNAs (miRNAs) are present in the circulation sparked interest in their use as potential biomarkers. In this review, we will summarize the latest findings on circulating miRNAs and cardiovascular disease but also discuss analytical challenges. While research on circulating miRNAs is still in its infancy, high analytical standards in statistics and study design are a prerequisite to obtain robust data and avoid repeating the mistakes of the early genetic association studies. Otherwise, studies tend to get published because of their novelty despite low numbers, poorly matched cases and controls and no multivariate adjustment for conventional risk factors. Research on circulating miRNAs can only progress by bringing more statistical rigour to bear in this field and by evaluating changes of individual miRNAs in the context of the overall miRNA network. Such miRNA signatures may have better diagnostic and prognostic value.

https://kclpure.kcl.ac.uk/portal/en/publications/profiling-of-circulating-micrornas(ca9e1d4a-f696-44f9-8024-8acd16f4628e).html

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March 2012
3 Reads

Review focus on the role of microRNA in cardiovascular biology and disease.

Cardiovasc Res 2012 Mar 7;93(4):543-4. Epub 2012 Feb 7.

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http://dx.doi.org/10.1093/cvr/cvs085DOI Listing
March 2012
5 Reads
19 Citations
5.940 Impact Factor

The -omics era: proteomics and lipidomics in vascular research.

Atherosclerosis 2012 Mar 2;221(1):12-7. Epub 2011 Oct 2.

King's British Heart Foundation Centre, King's College London, UK.

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http://dx.doi.org/10.1016/j.atherosclerosis.2011.09.043DOI Listing
March 2012
9 Reads
10 Citations
3.990 Impact Factor

Atheroprotective communication between endothelial cells and smooth muscle cells through miRNAs.

Nat Cell Biol 2012 Feb 12;14(3):249-56. Epub 2012 Feb 12.

Institute of Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe-University Hospital, 60590 Frankfurt, Germany.

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http://dx.doi.org/10.1038/ncb2441DOI Listing
February 2012
10 Reads
307 Citations
19.680 Impact Factor

Proteomics analysis of cardiac extracellular matrix remodeling in a porcine model of ischemia/reperfusion injury.

Circulation 2012 Feb 18;125(6):789-802. Epub 2012 Jan 18.

King's British Heart Foundation Centre, King's College London, 125 Coldharbour Lane, London, UK.

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http://dx.doi.org/10.1161/CIRCULATIONAHA.111.056952DOI Listing
February 2012
12 Reads
53 Citations
14.430 Impact Factor

MicroRNAs in vascular and metabolic disease.

Circ Res 2012 Feb;110(3):508-22

King's British Heart Foundation Centre, King’s College London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.111.247445DOI Listing
February 2012
26 Reads
61 Citations
11.020 Impact Factor

MicroRNAs in Vascular and Metabolic Disease

Circulation Research

Recent findings demonstrated the importance of microRNAs (miRNAs) in the vasculature and the orchestration of lipid metabolism and glucose homeostasis. MiRNA networks represent an additional layer of regulation for gene expression that absorbs perturbations and ensures the robustness of biological systems. This function is very elegantly demonstrated in cholesterol metabolism where miRNAs reducing cellular cholesterol export are embedded in the very same genes that increase cholesterol synthesis. Often their alteration does not affect normal development but changes under stress conditions and in disease. A detailed understanding of the molecular and cellular mechanisms of miRNA-mediated effects on metabolism and vascular pathophysiology could pave the way for the development of novel diagnostic markers and therapeutic approaches. In the first part of this review, we summarize the role of miRNAs in vascular and metabolic diseases and explore potential confounding effects by platelet miRNAs in preclinical models of cardiovascular disease. In the second part, we discuss experimental strategies for miRNA target identification and the challenges in attributing miRNA effects to specific cell types and single targets. (Circ Res. 2012;110:508-522.)

https://kclpure.kcl.ac.uk/portal/en/publications/micrornas-in-vascular-and-metabolic-disease(e57fa6ae-50cf-4d9c-b5db-5a568f5caadd).html

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February 2012
2 Reads

Pathogenesis of Varicose Veins

Journal of Vascular and Interventional Radiology

Despite the high prevalence of varicose veins and the recent surge in research on the condition, the precise mechanisms underlying their development remain uncertain. In the past decade, there has been a shift from initial theories based on purely mechanical factors to hypotheses pointing to complex molecular changes causing histologic alterations in the vessel wall and extracellular matrix. Despite progress in understanding the molecular aspects of venous insufficiency, therapies for symptomatic varicose veins are directed toward anatomic and physical interventions. The present report reviews current evidence identifying the underlying biochemical alterations in the pathogenesis of varicose veins.

https://kclpure.kcl.ac.uk/portal/en/publications/pathogenesis-of-varicose-veins(d5624f07-13dd-4ebc-955a-e14c260c1358).html

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January 2012
3 Reads

Pathogenesis of varicose veins.

J Vasc Interv Radiol 2012 Jan 26;23(1):33-9; quiz 40. Epub 2011 Oct 26.

Division of Vascular Imaging and Intervention, Massachusetts General Hospital, Harvard Medical School, 55 Fruit St, 290 Gray/Bigelow, Boston, MA 02114, USA.

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http://dx.doi.org/10.1016/j.jvir.2011.09.010DOI Listing
January 2012
24 Reads
7 Citations
2.150 Impact Factor

Coupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction: systemic inflammation and aging - a mini-review.

Gerontology 2011 11;57(4):295-303. Epub 2010 Jun 11.

Cardiovascular Section, Department of Experimental Medicine, Division of Investigative Sciences, Imperial College London, London, UK.

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http://dx.doi.org/10.1159/000316577DOI Listing
November 2011
5 Reads
16 Citations
3.060 Impact Factor

Nitrosative protein oxidation is modulated during early endotoxemia.

Nitric Oxide 2011 Aug 2;25(2):118-24. Epub 2010 Dec 2.

King's College London, Department of Cardiology, Cardiovascular Division, The Rayne Institute, St. Thomas' Hospital, London SE1 7EH, UK.

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http://dx.doi.org/10.1016/j.niox.2010.11.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3600856PMC
August 2011
4 Reads
7 Citations
3.520 Impact Factor

Extracellular matrix composition and remodeling in human abdominal aortic aneurysms: a proteomics approach.

Mol Cell Proteomics 2011 Aug 18;10(8):M111.008128. Epub 2011 May 18.

King's British Heart Foundation Centre, King's College London, London, UK.

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http://dx.doi.org/10.1074/mcp.M111.008128DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3149094PMC
August 2011
7 Reads
49 Citations
6.560 Impact Factor

Chromobox protein homolog 3 is essential for stem cell differentiation to smooth muscles in vitro and in embryonic arteriogenesis.

Arterioscler Thromb Vasc Biol 2011 Aug 9;31(8):1842-52. Epub 2011 Jun 9.

Centre for Clinical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom.

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http://dx.doi.org/10.1161/ATVBAHA.111.230110DOI Listing
August 2011
8 Reads
7 Citations
6.000 Impact Factor

Recent highlights of metabolomics in cardiovascular research.

Authors:
Manuel Mayr

Circ Cardiovasc Genet 2011 Aug;4(4):463-4

British Heart Foundation Centre, King's College London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCGENETICS.111.961003DOI Listing
August 2011
4 Reads
4 Citations
5.340 Impact Factor

Substrate modifications precede the development of atrial fibrillation after cardiac surgery: a proteomic study.

Ann Thorac Surg 2011 Jul;92(1):104-10

Department of Cardiothoracic Surgery, St. George's Hospital, and King's College, London, United Kingdom.

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http://dx.doi.org/10.1016/j.athoracsur.2011.03.071DOI Listing
July 2011
6 Reads
5 Citations
3.850 Impact Factor

From bench to bedside: what physicians need to know about endothelial progenitor cells.

Mayr M, Niederseer D, Niebauer J, The American journal of medicine, 2011, vol. 124, no. 6, pp. 489-497

http://europepmc.org/abstract/med/21605723

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July 2011
1 Read

Calcium regulates key components of vascular smooth muscle cell-derived matrix vesicles to enhance mineralization.

Circ Res 2011 Jun 12;109(1):e1-12. Epub 2011 May 12.

British Heart Foundation Centre, Cardiovascular Division, Kings College London, London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.110.238808DOI Listing
June 2011
26 Reads
70 Citations
11.020 Impact Factor

Comparative lipidomics profiling of human atherosclerotic plaques.

Circ Cardiovasc Genet 2011 Jun 21;4(3):232-42. Epub 2011 Apr 21.

King's British Heart Foundation Centre, King's College, London, UK.

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http://dx.doi.org/10.1161/CIRCGENETICS.110.959098DOI Listing
June 2011
11 Reads
29 Citations
5.340 Impact Factor

Cardiovascular stem cells revisited.

J Mol Cell Cardiol 2011 Feb;50(2):257

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http://dx.doi.org/10.1016/j.yjmcc.2011.01.003DOI Listing
February 2011
5 Reads
4.660 Impact Factor

Proteomics A Reality-Check for Putative Stem Cells

Circulation Research

The concept of using stem cells for cardiovascular repair holds great potential, but uncertainties in preclinical experiments must be addressed before their therapeutic application. Contemporary proteomic techniques can help to characterize cell preparations more thoroughly and identify some of the potential causes that may lead to a high failure rate in clinical trials. The first part of this review discusses the broader application of proteomics to stem cell research by providing an overview of the main proteomic technologies and how they might help the translation of stem cell therapy. The second part focuses on the controversy about endothelial progenitor cells (EPCs) and raises cautionary flags for marker assignment and assessment of cell purity. A proteomics-led approach in early outgrowth EPCs has already raised the awareness that markers used to define their endothelial potential may arise from an uptake of platelet proteins. A platelet microparticle-related transfer of endothelial characteristics to mononuclear cells can result in a misinterpretation of the assay. The necessity to perform counterstaining for platelet markers in this setting is not fully appreciated. Similarly, the presence of platelets and platelet microparticles is not taken into consideration when functional improvements are directly attributed to EPCs, whereas saline solutions or plain medium serve as controls. Thus, proteomics shed new light on the caveats of a common stem cell assay in cardiovascular research, which might explain some of the inconsistencies in the field. (Circ Res. 2011;108:499-511.)

https://kclpure.kcl.ac.uk/portal/en/publications/proteomics-a-realitycheck-for-putative-stem-cells(2db4e9b1-46cb-43a2-bd1f-d059024adb2d).html

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February 2011
1 Read

Proteomic characterization of human early pro-angiogenic cells.

J Mol Cell Cardiol 2011 Feb 13;50(2):333-6. Epub 2010 Dec 13.

Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Frankfurt, Germany.

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http://dx.doi.org/10.1016/j.yjmcc.2010.11.022DOI Listing
February 2011
8 Reads
11 Citations
4.660 Impact Factor

Proteomics: a reality-check for putative stem cells.

Circ Res 2011 Feb;108(4):499-511

King's British Heart Foundation Centre, King's College London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.110.226902DOI Listing
February 2011
7 Reads
7 Citations
11.020 Impact Factor

Redox regulation of soluble epoxide hydrolase by 15-deoxy-delta-prostaglandin J2 controls coronary hypoxic vasodilation.

Circ Res 2011 Feb 16;108(3):324-34. Epub 2010 Dec 16.

King's College London, Cardiovascular Division, The Rayne Institute, St Thomas Hospital, London, SE1 7EH, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.110.235879DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3259859PMC
February 2011
10 Reads
13 Citations
11.020 Impact Factor

Preoperative high-dose atorvastatin for prevention of atrial fibrillation after cardiac surgery: a randomized controlled trial.

J Thorac Cardiovasc Surg 2011 Jan 10;141(1):244-8. Epub 2010 Jul 10.

Department of Cardiothoracic Surgery, St George's Hospital, London, United Kingdom.

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http://dx.doi.org/10.1016/j.jtcvs.2010.06.006DOI Listing
January 2011
11 Reads
2 Citations
4.170 Impact Factor

Highlights from the 2010 BAS/BSCR spring meeting: New Frontiers in Cardiovascular Research.

Expert Rev Proteomics 2010 Dec;7(6):811-3

King's BHF Centre, King's College London, 125 Coldharbour Lane, London, UK.

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http://dx.doi.org/10.1586/epr.10.94DOI Listing
December 2010
3 Reads
2.900 Impact Factor

Proteomics characterization of extracellular space components in the human aorta.

Mol Cell Proteomics 2010 Sep 15;9(9):2048-62. Epub 2010 Jun 15.

King's British Heart Foundation Centre, King's College, London, United Kingdom.

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http://dx.doi.org/10.1074/mcp.M110.001693DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2938114PMC
September 2010
2 Reads
68 Citations
6.560 Impact Factor

Plasma microRNA profiling reveals loss of endothelial miR-126 and other microRNAs in type 2 diabetes.

Circ Res 2010 Sep 22;107(6):810-7. Epub 2010 Jul 22.

King's British Heart Foundation Centre, King's College London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.110.226357DOI Listing
September 2010
25 Reads
307 Citations
11.020 Impact Factor

Comparative proteomics profiling reveals role of smooth muscle progenitors in extracellular matrix production.

Arterioscler Thromb Vasc Biol 2010 Jul 29;30(7):1325-32. Epub 2010 Apr 29.

Department of Cardiology, Phoenix VA Health Care System, Phoenix, AZ, USA.

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http://dx.doi.org/10.1161/ATVBAHA.110.204651DOI Listing
July 2010
8 Reads
10 Citations
6.000 Impact Factor

Short communication: asymmetric dimethylarginine impairs angiogenic progenitor cell function in patients with coronary artery disease through a microRNA-21-dependent mechanism.

Circ Res 2010 Jul 20;107(1):138-43. Epub 2010 May 20.

Institute of Molecular and Translational Therapeutic Strategies, Hannover Medical School, Hannover, Germany.

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http://dx.doi.org/10.1161/CIRCRESAHA.110.216770DOI Listing
July 2010
7 Reads
43 Citations
11.020 Impact Factor

Asymmetric dimethylarginine impairs angiogenic progenitor cell function in patients with coronary artery disease through a microRNA-21-dependent mechanism

Circulation Research

Rationale: The endogenous nitric oxide synthase inhibitor asymmetrical dimethylarginine (ADMA) is increased in patients with coronary artery disease and may regulate function of circulating angiogenic progenitor cells (APCs) by small regulatory RNAs. Objectives: To study the role of microRNAs in ADMA-mediated impairment of APCs. Methods and Results: By using microarray analyses, we established microRNA expression profiles of human APCs. We used ADMA to induce APC dysfunction and found 16 deregulated microRNAs. We focused on miR-21, which was 3-fold upregulated by ADMA treatment. Overexpression of miR-21 in human APCs impaired migratory capacity. To identify regulated miR-21 targets, we used proteome analysis, using difference in-gel electrophoresis followed by mass spectrometric analysis of regulated proteins. We found that transfection of miR-21 precursors significantly repressed superoxide dismutase 2 in APCs, which resulted in increased intracellular reactive oxygen species concentration and impaired nitric oxide bioavailability. MiR-21 further repressed sprouty-2, leading to Erk Map kinase-dependent reactive oxygen species formation and APC migratory defects. Small interference RNA-mediated superoxide dismutase 2 or sprouty-2 reduction also increased reactive oxygen species formation and impaired APC migratory capacity. ADMA-mediated reactive oxygen species formation and APC dysfunction was rescued by miR-21 blockade. APCs from patients with coronary artery disease and high ADMA plasma levels displayed >4-fold elevated miR-21 levels, low superoxide dismutase 2 expression, and impaired migratory capacity, which could be normalized by miR-21 antagonism. Conclusions: We identified a novel miR-21-dependent mechanism of ADMA-mediated APC dysfunction. MiR-21 antagonism therefore emerges as an interesting strategy to improve dysfunctional APCs in patients with coronary artery disease. (Circ Res. 2010; 107: 138-143.)

https://kclpure.kcl.ac.uk/portal/en/publications/asymmetric-dimethylarginine-impairs-angiogenic-progenitor-cell-function-in-patients-with-coronary-artery-disease-through-a-microrna21dependent-mechanism(be0eeaa0-3880-4ad9-b3cc-cd3894ac022d).html

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July 2010
2 Reads

Phenotyping transgenic animals--an integrated readout of pathophysiology by combining proteomics and metabolomics with cardiovascular imaging.

J Mol Cell Cardiol 2010 Apr 16;48(4):571-3. Epub 2009 Dec 16.

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http://dx.doi.org/10.1016/j.yjmcc.2009.12.001DOI Listing
April 2010
3 Reads
1 Citation
4.660 Impact Factor

Histone deacetylase 7 controls endothelial cell growth through modulation of beta-catenin.

Circ Res 2010 Apr 11;106(7):1202-11. Epub 2010 Mar 11.

Cardiovascular Division, King's College London British Heart Foundation Centre, London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.109.213165DOI Listing
April 2010
7 Reads
38 Citations
11.020 Impact Factor

Proteomics analysis of the cardiac myofilament subproteome reveals dynamic alterations in phosphatase subunit distribution.

Mol Cell Proteomics 2010 Mar 27;9(3):497-509. Epub 2009 Dec 27.

King's British Heart Foundation Centre, King's College London, London SE5 9NU, United Kingdom.

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http://dx.doi.org/10.1074/mcp.M900275-MCP200DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849712PMC
March 2010
28 Reads
28 Citations
6.560 Impact Factor

Identification of cardiac myosin-binding protein C as a candidate biomarker of myocardial infarction by proteomics analysis.

Mol Cell Proteomics 2009 Dec 31;8(12):2687-99. Epub 2009 Aug 31.

King's College London British Heart Foundation Centre, London, United Kingdom.

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http://dx.doi.org/10.1074/mcp.M900176-MCP200DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2816024PMC
December 2009
3 Reads
23 Citations
6.560 Impact Factor

Proteomic analysis of the secretome of human umbilical vein endothelial cells using a combination of free-flow electrophoresis and nanoflow LC-MS/MS.

Proteomics 2009 Nov;9(21):4991-6

Pharmacology Laboratory (CDB), Hospital Clinic, IDIBAPS, Barcelona University, CIBERehd, Barcelona, Spain.

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http://dx.doi.org/10.1002/pmic.200900065DOI Listing
November 2009
24 Reads
14 Citations
3.810 Impact Factor

Proteomics, metabolomics, and immunomics on microparticles derived from human atherosclerotic plaques.

Circ Cardiovasc Genet 2009 Aug 14;2(4):379-88. Epub 2009 May 14.

Cardiovascular Division, King's BHF Centre of Research Excellence, King's College London, London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCGENETICS.108.842849DOI Listing
August 2009
8 Reads
29 Citations
5.340 Impact Factor

Asymmetric and symmetric dimethylarginines are of similar predictive value for cardiovascular risk in the general population.

Atherosclerosis 2009 Jul 12;205(1):261-5. Epub 2008 Nov 12.

Department of Neurology, Medical University Innsbruck, Innsbruck, Austria.

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http://dx.doi.org/10.1016/j.atherosclerosis.2008.10.040DOI Listing
July 2009
6 Reads
21 Citations
3.990 Impact Factor

Proteomic analysis reveals presence of platelet microparticles in endothelial progenitor cell cultures.

Blood 2009 Jul 15;114(3):723-32. Epub 2009 Apr 15.

King's British Heart Foundation Centre, King's College London, 125 Coldharbour Lane, London, United Kingdom.

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http://dx.doi.org/10.1182/blood-2009-02-205930DOI Listing
July 2009
19 Reads
66 Citations
10.450 Impact Factor

Proteomics of acute coronary syndromes.

Curr Atheroscler Rep 2009 May;11(3):188-95

Cardiovascular Division, The James Black Centre, King's College London School of Medicine, King's College London, 125 Coldharbour Lane, London SE59NU, United Kingdom.

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May 2009
6 Reads
11 Citations
3.420 Impact Factor

Proteomics identifies thymidine phosphorylase as a key regulator of the angiogenic potential of colony-forming units and endothelial progenitor cell cultures.

Circ Res 2009 Jan 20;104(1):32-40. Epub 2008 Nov 20.

Cardiovascular Division, King's College London School of Medicine, King's College London, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.108.182261DOI Listing
January 2009
11 Reads
32 Citations
11.020 Impact Factor

Metabolomics: ready for the prime time?

Authors:
Manuel Mayr

Circ Cardiovasc Genet 2008 Oct;1(1):58-65

Cardiovascular Division, King's College, London School of Medicine, King's College London, UK.

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http://dx.doi.org/10.1161/CIRCGENETICS.108.808329DOI Listing
October 2008
7 Reads
22 Citations
5.340 Impact Factor

Cardiovascular proteomics.

Proteomics Clin Appl 2008 Jun;2(6):785-6

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http://dx.doi.org/10.1002/prca.200890020DOI Listing
June 2008
6 Reads
1 Citation
2.680 Impact Factor

Proteomic analysis of secretory proteins and vesicles in vascular research.

Proteomics Clin Appl 2008 Jun;2(6):882-91

Cardiovascular Division, King's College London, London, UK.

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http://doi.wiley.com/10.1002/prca.200800040
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http://dx.doi.org/10.1002/prca.200800040DOI Listing
June 2008
7 Reads
6 Citations
2.680 Impact Factor

Proteomic and metabolomic analysis of smooth muscle cells derived from the arterial media and adventitial progenitors of apolipoprotein E-deficient mice.

Circ Res 2008 May 3;102(9):1046-56. Epub 2008 Apr 3.

Cardiovascular Division, The James Black Centre, King's College, University of London, 125 Coldharbour Ln, London SE5 9NU, United Kingdom.

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http://dx.doi.org/10.1161/CIRCRESAHA.108.174623DOI Listing
May 2008
10 Reads
16 Citations
11.020 Impact Factor

The paradox of hypoxic and oxidative stress in atherosclerosis.

J Am Coll Cardiol 2008 Apr;51(13):1266-7

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http://dx.doi.org/10.1016/j.jacc.2008.01.005DOI Listing
April 2008
13 Reads
10 Citations
16.500 Impact Factor

Combined metabolomic and proteomic analysis of human atrial fibrillation.

J Am Coll Cardiol 2008 Feb;51(5):585-94

Cardiovascular Division, King's College, London, United Kingdom.

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http://dx.doi.org/10.1016/j.jacc.2007.09.055DOI Listing
February 2008
5 Reads
1 Citation
16.500 Impact Factor

Endothelial progenitor cells, late stent thrombosis and delayed re-endothelialisation.

EuroIntervention 2008 Jan;3(4):518-25

Department of Cardiology, King's College Hospital, Denmark Hill, London, United Kingdom.

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January 2008
6 Reads
3.770 Impact Factor

Integrated membrane protein analysis of mature and embryonic stem cell-derived smooth muscle cells using a novel combination of CyDye/biotin labeling.

Mol Cell Proteomics 2007 Oct 11;6(10):1788-97. Epub 2007 Jul 11.

Cardiovascular Division, King's College London School of Medicine, Kings College London, University of London, SE5 9NU London, United Kingdom.

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http://dx.doi.org/10.1074/mcp.M600433-MCP200DOI Listing
October 2007
8 Reads
6 Citations
6.560 Impact Factor

Protein kinase D selectively targets cardiac troponin I and regulates myofilament Ca2+ sensitivity in ventricular myocytes.

Circ Res 2007 Mar 22;100(6):864-73. Epub 2007 Feb 22.

Cardiovascular Division, King's College London, London, UK.

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http://dx.doi.org/10.1161/01.RES.0000260809.15393.faDOI Listing
March 2007
20 Reads
49 Citations
11.020 Impact Factor

Proteomic and metabolomics combined in cardiovascular research

TRENDS IN CARDIOVASCULAR MEDICINE

Proteomics and metabolomics offer a nonbiased suite of tools to address pathophysiologic mechanisms from various levels by integrating signal transduction, cellular metabolism, and phenotype analysis. To link alterations of cellular proteins to metabolism and function, we have recently combined proteomic and metabolomic techniques. Examples, including genetic manipulation, ischemic preconditioning, atherosclerosis, and stem cell differentiation, are discussed to illustrate how the combination of these updated technologies may advance our understanding of cardiovascular biology. (c) 2007, Elsevier Inc

https://kclpure.kcl.ac.uk/portal/en/publications/proteomic-and-metabolomics-combined-in-cardiovascular-research(2b0d314d-6b5e-4596-9f9e-fc9b75453629).html

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March 2007
1 Read

Proteomics and metabolomics combined in cardiovascular research.

Trends Cardiovasc Med 2007 Feb;17(2):43-8

Cardiovascular Division, King's College, London SE5 9NU, UK.

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http://dx.doi.org/10.1016/j.tcm.2006.11.004DOI Listing
February 2007
4 Reads
15 Citations
2.910 Impact Factor

Proteomic analysis reveals higher demand for antioxidant protection in embryonic stem cell-derived smooth muscle cells.

Proteomics 2006 Dec;6(24):6437-46

Cardiovascular Division, School of Medicine, King's College, University of London, UK.

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http://dx.doi.org/10.1002/pmic.200600351DOI Listing
December 2006
5 Reads
4 Citations
3.810 Impact Factor

The role of oxidant stress in angiotensin II-mediated contraction of human resistance arteries in the state of health and the presence of cardiovascular disease.

Vascul Pharmacol 2006 Dec 14;45(6):395-9. Epub 2006 Jun 14.

Department of Pharmacology and Clinical Pharmacology, St. George's, University of London, London, SW17 0RE, UK.

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http://dx.doi.org/10.1016/j.vph.2006.06.001DOI Listing
December 2006
8 Reads
3 Citations
4.620 Impact Factor

Proteomics-based Development of Biomarkers in Cardiovascular Disease: Mechanistic, Clinical, and Therapeutic Insights

MOLECULAR AND CELLULAR PROTEOMICS

Cardiovascular disease remains a paramount focus of basic science and clinical investigation throughout the developed world, although the demographics have changed considerably in the later half of the 20th century. Atherosclerotic cardiovascular disease, especially ischemic heart disease, has emerged as the major concern, while rheumatic fever and its cardiac sequelae have been superseded by congenital heart disease. Understanding these disease states and their perturbations requires clarification of mechanistic changes in organ phenotype over time, the influence of genetic variations, and the effects of pharmacologic, surgical, and interventional treatment. These requirements have been addressed, in part, by genetic, biochemical, and system approaches. It is clear, however, that knowledge of the DNA sequence, although essential, is not sufficient. A more meaningful understanding of gene expression can be achieved through characterization of the products of that expression, the proteins that are the essential biological determinants of disease phenotype. The ultimate phenotype of cell, organ, and organism is reflected in the instantaneous proteomic profile; similarly changes in human states of health are the result of changes in the proteomes of individual patients over time in response to endogenous and/or external stimuli. The advent of novel proteomic approaches to investigate the complexity of human illness promises to shed new light on the pathogenesis of a broad range of cardiovascular diseases. These inferences are multifaceted and include the commonly recognized role of proteomics in characterizing biomarkers and biosignatures for the prognosis and diagnosis of disease, the capability of these technologies of revealing information regarding functional subproteomes of organelles and networks in the heart and vasculature, and the importance of proteomics in defining changes in these functional subproteomes to guide future therapy. The central focus of this review is to discuss the importance of proteomics as a non-biased tool for protein discovery. We explore the role of proteomics for hypothesis-driven research into cellular organelle status, and we discuss how this approach facilitates an understanding of the function of the cell in normal and diseased states. Lastly we present a review of proteomics as a tool for biomarker development and lay out a vision for how this technology promises to facilitate distinct biomarker development.

https://kclpure.kcl.ac.uk/portal/en/publications/proteomicsbased-development-of-biomarkers-in-cardiovascular-disease-mechanistic-clinical-and-therapeutic-insights(2e6074eb-0f7f-43ee-ba6c-6aadc0fc45ef).html

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October 2006

Oxidized low-density lipoprotein autoantibodies, chronic infections, and carotid atherosclerosis in a population-based study

Journal of the American College of Cardiology

OBJECTIVES: We investigated whether associations exist between immune reactions to oxidized low-density lipoproteins (OxLDLs), chronic infections, and carotid atherosclerosis as quantified by ultrasound. BACKGROUND: Atherosclerosis is a chronic immuno-inflammatory disease wherein both oxidized lipids and infectious agents are incriminated as possible contributors. METHODS: We measured immunoglobulin (Ig)G and IgM autoantibody titers to copper-oxidized-LDL and malondialdehyde-LDL (OxLDL-AB), IgG and IgM apolipoprotein B-100-immune complexes (ApoB-IC), and titers of antibodies to Escherichia coli and chlamydial lipopolysaccharide (LPS), mycobacterial heat shock protein 65 (mHSP65), Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus and evaluated their relationship to cardiovascular risk factors, chronic infections, and incident/progressive carotid atherosclerosis in the Bruneck study. RESULTS: The OxLDL-AB and ApoB-IC levels remained stable over time as indicated by strong correlations between 1995 and 2000 measurements (p <0.001 each). Significant associations existed between all OxLDL markers and antibody titers to pathogens, especially to E. coli-LPS and mHSP65. Both OxLDL-AB and ApoB-IC levels showed a rise with increasing pathogen burden. Notably, OxLDL-ABs were also elevated in subjects with chronic infection as defined by clinical criteria. Titers of IgG, but not IgM, OxLDL-AB, or ApoB-IC inversely correlated with total cholesterol, LDL cholesterol, and apoB concentrations. The IgG OxLDL markers were positively and IgM markers were inversely associated with incident and progressive carotid atherosclerosis in univariate analyses but were not independent predictors in multivariate analyses. CONCLUSIONS: Our study provides evidence for an association between human oxLDL markers and chronic infections. Moreover, in this population-based study, neither IgG nor IgM OxLDL autoantibodies were independently predictive of atherosclerosis progression in the carotid arteries.

https://kclpure.kcl.ac.uk/portal/en/publications/oxidized-lowdensity-lipoprotein-autoantibodies-chronic-infections-and-carotid-atherosclerosis-in-a-populationbased-study(ca80bd0f-b6db-40db-b066-79fdbf6b8054).html

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June 2006
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Oxidized phospholipids predict the presence and progression of carotid and femoral atherosclerosis and symptomatic cardiovascular disease - Five-year prospective results from the Bruneck study

Journal of the American College of Cardiology

OBJECTIVES The purpose of this work was to determine the predictive value of oxidized phospholipids (OxPLs) present on apotipoprotein B-100 particles (apoB) in carotid and femoral atherosclerosis. BACKGROUND The OxPLs are pro-inflammatory and pro-atherogenic and may be detected using the antibody E06 (OxPL/apoB). METHODS The Bruneck study is a prospective population-based survey of 40- to 79-year-old men and women initiated in 1990. Plasma levels of OxPL/apoB and lipoprotein (a) [Lp(a)] were measured in 765 of 826 (92.6%) and 671 of 684 (98.1%) subjects alive in 1995 and 2000, respectively, and correlated with ultrasound measures of carotid and femoral atherosclerosis. RESULTS The distribution of the OxPL/apoB levels was skewed to lower levels and nearly identical to Lp(a) levels. The OxPL/apoB and Lp(a) levels were highly correlated (r = 0.87, p <0.001), and displayed long-term stability and lacked correlations with most cardiovascular risk factors and lifestyle variables. The number of apolipoprotein (a) kringle IV-2 repeats was inversely related to Lp(a) mass (r = -0.48, p <0.001) and OxPUapoB levels (r = -0.46, p <0.001). In multivariable analysis, OxPL/apoB levels were strongly and significantly associated with the presence, extent, and development (1995 to 2000) of carotid and femoral atherosclerosis and predicted the presence of symptomatic cardiovascular disease. Both OxPL/apoB and Lp(a) levels showed similar associations with atherosclerosis severity and progression, suggesting a common biological influence on atherogenesis. CONCLUSIONS This study suggests that pro-inflammatory oxidized phosphotipids, present primarily on Lp(a), are significant predictors of the presence and extent of carotid and femoral atherosclerosis, development of new lesions, and increased risk of cardiovascular events. The OxPL biomarkers may provide valuable insights into diagnosing and monitoring cardiovascular disease

https://kclpure.kcl.ac.uk/portal/en/publications/oxidized-phospholipids-predict-the-presence-and-progression-of-carotid-and-femoral-atherosclerosis-and-symptomatic-cardiovascular-disease--fiveyear-prospective-results-from-the-bruneck-study(5f55e71a-52d1-4cd8-8fcd-593eb58aa7c3).html

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June 2006
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Association of serum-soluble heat shock protein 60 with carotid atherosclerosis - Clinical significance determined in a follow-up study

Stroke

Background and Purpose - Previous work has shown that soluble heat shock protein 60 (HSP60; sHSP60), present in circulating blood, is associated with carotid atherosclerosis. In the current evaluation, we tested the hypothesis that sHSP60 levels are associated with the progression of carotid arteriosclerosis, prospectively. Methods - The association of sHSP60 with early atherogenesis (5-year development and progression of nonstenotic carotid plaques) was investigated as part of the population-based prospective Bruneck Study. The current study focused on the follow-up period between 1995 and 2000 and, thus, included 684 subjects. Results - sHSP60 levels measured in 1995 and 2000 were highly correlated (r = 0.40; P <0.001), indicating consistency over a 5-year period. Circulating HSP60 levels were significantly correlated with antilipopolysaccharide and anti-HSP60 antibodies. It was also elevated in subjects with chronic infection (top quintile group of HSP60, among subjects with and without chronic infection: 23.8% versus 17.0%; P = 0.003 after adjustment for age and sex). HSP60 levels were significantly associated with early atherogenesis, both in the entire population (multivariate odds ratio, for a comparison between quintile group V versus I + II: 2.0 [1.2 to 3.5] and the subgroup free of atherosclerosis at the 1995 baseline: 3.8 [1.6 to 8.9]). The risk of early atherogenesis was additionally amplified when high-sHSP60 and chronic infection were present together. Conclusions - Our study provides the first prospective data confirming an association between high levels of sHSP60 and early carotid atherosclerosis. This possibly indicates an involvement of sHSP60 in activating proinflammatory processes associated with early vessel pathology

https://kclpure.kcl.ac.uk/portal/en/publications/association-of-serumsoluble-heat-shock-protein-60-with-carotid-atherosclerosis--clinical-significance-determined-in-a-followup-study(11bfa269-9714-45b6-a1ec-7458ea4eaef2).html

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2005
1 Read

Proteomic dataset of mouse aortic smooth muscle cells

Proteomics

In an accompanying study (in this issue, DOI 10.1002/pmic.200402044), we have characterised the proteome of Sca-1(+) progenitor cells, which may function as precursors of vascular smooth muscle cells (SMCs). In the present study, we have analysed and mapped protein expression in aortic SMCs of mice, using 2-DE, MALDI-TOF MS and MS/MS. The 2-D system comprised a non-linear immobilised pH 3-10 gradient in the first dimension (separating proteins with pI values of pH 3-10), and 12%T SDS-PAGE in the second dimension (separating proteins in the range 15 000-150 000 Da). Of the 2400 spots visualised, a subset of 267 protein spots was analysed, with 235 protein spots being identified corresponding to 154 unique proteins. The data presented here are the first map of aortic SMCs and the most extensive analysis of SMC proteins published so far. This valuable tool should provide a basis for comparative studies of protein expression in vascular smooth muscle of transgenic mice and is available on our website hhtp://www.vascular-proteomics.com

https://kclpure.kcl.ac.uk/portal/en/publications/proteomic-dataset-of-mouse-aortic-smooth-muscle-cells(29c0b812-1063-4e3f-8cb6-34efb3d73c67).html

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December 2005
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Proteomic dataset of Sca-1(+) progenitor cells

Proteomics

Embryonic stem cells (ES cells) can differentiate into endothelial cells and smooth muscle cells (SMCs), which participate in vascular angiogenesis. In this study, we differentiated mouse ES cells into Sca-1(+) cells, which have the potential to serve as vascular progenitor cells, and mapped their proteome by 2-DE using a pH 3-10 non-linear gradient and 12% SDS-polyacrylamide gels. A subset of 300 protein spots was analysed and mapped, with 241 protein spots being identified by their PMF using MALDI-TOF MS or by partial amino acid sequencing using MS/MS. Our protein map is the first of Sca-1(+) progenitor cells and will facilitate the identification of proteins differentially expressed during stem cell differentiation. The proteome of adult arterial SMCs is described in an accompanying paper (in this issue, DOI 10.1002/pmic.200402045). All data are made accessible on our website http://www.vascular-proteomics.com

https://kclpure.kcl.ac.uk/portal/en/publications/proteomic-dataset-of-sca1-progenitor-cells(a541ecbe-b656-4054-878d-d6785c2bf5b8).html

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December 2005
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Proteomic dataset of Sca-1+ progenitor cells.

Yin X, Mayr M, Xiao Q, Mayr U, Tarelli E, Wait R, Wang W, Xu Q, Proteomics, 2005, vol. 5, no. 17, pp. 4533-4545

http://europepmc.org/abstract/med/16240289

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December 2005
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Role of oxidative stress in angiotensin-II mediated contraction of human conduit arteries in patients with cardiovascular disease

VASCULAR PHARMACOLOGY

Background: Angiotensin pi is a powerful vasoconstrictor involved in the development of high blood pressure and in the regulation of cardiovascular growth. Recent reports have suggested that in addition to the classical pathways involved in transducing responses to receptor activation, formation of reactive oxygen species by angiotensin pi may also be involved. We investigated the importance of oxidative stress in angiotensin pi induced contraction in human conduit arteries from patients with cardiovascular disease. Methods and results: Isometric contraction studies using human radial arteries entailed probes modulating the redox-dependent reactions to define the oxidative pathways involved in angiotensin pi contraction. In situ oxidative fluorescence was employed to detect immediate superoxide tissue production in radial and internal mammary arteries. Treatment with TEMPOL, human superoxide dismutase, diphenyleneiodonium, oxypurinol, NG-monomethyl L-arginine considerably decreased contractile response to angiotensin pi in radial arteries. Similarly, angiotensin pi-stimulated arterial superoxide production was reduced in the presence of the above inhibitors. On the contrary, used as controls, norepinephrine vasoconstriction was not associated with increase of superoxide and neither ciprofloxacin nor aminophylline altered basal or angiotensin pi induced superoxide generation. Conclusions: Our findings provide evidence for the role of oxidative pathways in contractile response of human conduit arteries to angiotensin pi. Angiotensin pi induced superoxide anion production may be mediated by multiple inter-dependent rate-limiting enzymes in both types of artery. Our studies may have important implication for future therapeutic approaches involving inhibition of angiotensin pi mediated superoxide generation in hypertension and prevention of cardiovascular disease. Condensed abstract: We studied the role of oxidant species in contraction responses to angiotensin pi in human conduit arteries. Treating radial artery segments with the anti-oxidants with a range of inhibitors, affecting the redox dependent pathways, markedly reduced contraction to angiotensin pi. In parallel experiments, oxidative fluorescence was assessed and compared in human radial and internal mammary artery. Angiotensin pi induced superoxide anion production may be mediated by multiple inter-dependent rate-limiting enzymes in both types of artery. (c) 2005 Elsevier Inc. All rights reserved

https://kclpure.kcl.ac.uk/portal/en/publications/role-of-oxidative-stress-in-angiotensinii-mediated-contraction-of-human-conduit-arteries-in-patients-with-cardiovascular-disease(9dcecc4e-542a-4349-8a45-60b70d582152).html

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October 2005

Proteomic and metabolomic analyses of atherosclerotic vessels from apolipoprotein E-deficient mice reveal alterations in inflammation, oxidative stress, and energy metabolism

Arteriosclerosis, Thrombosis, and Vascular Biology

OBJECTIVE: Proteomics and metabolomics are emerging technologies to study molecular mechanisms of diseases. We applied these techniques to identify protein and metabolite changes in vessels of apolipoprotein E(-/-) mice on normal chow diet. METHODS AND RESULTS: Using 2-dimensional gel electrophoresis and mass spectrometry, we identified 79 protein species that were altered during various stages of atherogenesis. Immunoglobulin deposition, redox imbalance, and impaired energy metabolism preceded lesion formation in apolipoprotein E(-/-) mice. Oxidative stress in the vasculature was reflected by the oxidation status of 1-Cys peroxiredoxin and correlated to the extent of lesion formation in 12-month-old apolipoprotein E(-/-) mice. Nuclear magnetic resonance spectroscopy revealed a decline in alanine and a depletion of the adenosine nucleotide pool in vessels of 10-week-old apolipoprotein E(-/-) mice. Attenuation of lesion formation was associated with alterations of NADPH generating malic enzyme, which provides reducing equivalents for lipid synthesis and glutathione recycling, and successful replenishment of the vascular energy pool. CONCLUSIONS: Our study provides the most comprehensive dataset of protein and metabolite changes during atherogenesis published so far and highlights potential associations of immune-inflammatory responses, oxidative stress, and energy metabolism.

https://kclpure.kcl.ac.uk/portal/en/publications/proteomic-and-metabolomic-analyses-of-atherosclerotic-vessels-from-apolipoprotein-edeficient-mice-reveal-alterations-in-inflammation-oxidative-stress-and-energy-metabolism(bb3d5cca-33f9-4e45-9241-3581861e55d6).html

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October 2005
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Vascular proteomics: linking proteomic and metabolomic changes.

Mayr M, Mayr U, Chung YL, Yin X, Griffiths JR, Xu Q, Proteomics, 2004, vol. 4, no. 12, pp. 3751-3761

http://europepmc.org/abstract/med/15540213

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2004
2 Reads

Loss of PKC-delta alters cardiac metabolism

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY

PKC-delta is believed to play an essential role in cardiomyocyte growth. In the present study, we investigated the effect of PKC-delta on cardiac metabolism using PKC-delta knockout mice generated in our laboratories. Proteomic analysis of heart protein extracts revealed profound changes in enzymes related to energy metabolism: certain isoforms of glycolytic enzymes, e.g., lactate dehydrogenase and pyruvate kinase, were absent or decreased, whereas several enzymes involved in lipid metabolism, e.g., phosphorylated isoforms of acyl-CoA dehydrogenases, showed a marked increase in PKC-delta(-/-) hearts. Moreover, PKC-delta deficiency was associated with changes in antioxidants, namely, 1-Cys peroxiredoxin and selenium-binding protein 1, and posuranslational modifications of chaperones involved in cytoskeleton regulation, such as heat shock protein (HSP)20, HSP27. and the zeta-subunit of the cytosolic chaperone containing the T-complex polypeptide 1. High-resolution NMR analysis of cardiac metabolites confirmed a significant decrease in the ratio of glycolytic end products (alanine + lactate) to end products of lipid metabolism (acetate) in PKC-delta(-/-) hearts. Taken together, Our data demonstrate that loss of PKC-delta causes a shift from Glucose to lipid metabolism in murine hearts, and we provide a detailed description of the enzymatic changes on a proteomic level. The consequences of these metabolic alterations on sensitivity to myocardial ischemia are further explored in the accompanying paper (20).

https://kclpure.kcl.ac.uk/portal/en/publications/loss-of-pkcdelta-alters-cardiac-metabolism(04f97c2e-8967-44b5-9c66-491a87cd3ef3).html

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August 2004
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Ischemic preconditioning exaggerates cardiac damage in PKC-delta null mice

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY

Ischemic preconditioning confers cardiac protection during subsequent ischemia-reperfusion, in which protein kinase C (PKC) is believed to play an essential role, but controversial data exist concerning the PKC-delta isoform. In an accompanying study (26), we described metabolic changes in PKC-delta knockout mice. We now wanted to explore their effect on early preconditioning. Both PKC-delta(-/-) and PKC-delta(+/+) mice underwent three cycles of 5-min left descending artery occlusion/5-min reperfusion, followed by 30-min occlusion and 2-h reperfusion. Unexpectedly, preconditioning exaggerated ischemia-reperfusion injury in PKC-delta(-/-) mice. Whereas ischemic preconditioning increased superoxide anion production in PKC-delta(+/+) hearts, no increase in reactive oxygen species was observed in PKC-delta(-/-) hearts. Proteomic analysis of preconditioned PKC-delta(+/+) hearts revealed profound changes in enzymes related to energy metabolism, e.g., NADH dehydrogenase and ATP synthase, with partial fragmentation of these mitochondrial enzymes and of the E-2 component of the pyruvate dehydrogenase complex. Interestingly, fragmentation of mitochondrial enzymes was not observed in PKC-delta(-/-) hearts. High-resolution NMR analysis of cardiac metabolites demonstrated a similar rise of phosphocreatine in PKC-delta(+/+) and PKC-delta(-/-) hearts, but the preconditioning-induced increase in phosphocholine, alanine, carnitine, and glycine was restricted to PKC-delta(+/+) hearts, whereas lactate concentrations were higher in PKC-delta(-/-) hearts. Taken together, our results suggest that reactive oxygen species generated during ischemic preconditioning might alter mitochondrial metabolism by oxidizing key mitochondrial enzymes and that metabolic adaptation to preconditioning is impaired in PKC-delta(-/-) hearts.

https://kclpure.kcl.ac.uk/portal/en/publications/ischemic-preconditioning-exaggerates-cardiac-damage-in-pkcdelta-null-mice(29d6d442-1bf8-4fbf-aeef-b213a6da37ad).html

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August 2004
1 Read

Loss of PKC-delta alters cardiac metabolism.

Mayr M, Chung YL, Mayr U, McGregor E, Troy H, Baier G, Leitges M, Dunn MJ, Griffiths JR, Xu Q, American journal of physiology. Heart and circulatory physiology, 2004, vol. 287, no. 2, pp. H937-45

http://europepmc.org/abstract/med/15277208

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August 2004
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Cross-reactive B-cell epitopes of microbial and human heat shock protein 60/65 in atherosclerosis.

Perschinka H, Mayr M, Millonig G, Mayerl C, van der Zee R, Morrison SG, Morrison RP, Xu Q, Wick G, Arteriosclerosis, thrombosis, and vascular biology, 2003, vol. 23, no. 6, pp. 1060-1065

http://europepmc.org/abstract/med/12702515

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July 2003
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Increased risk of atherosclerosis is confined to CagA-positive Helicobacter pylori strains: prospective results from the Bruneck study.

Mayr M, Kiechl S, Mendall MA, Willeit J, Wick G, Xu Q, Stroke; a journal of cerebral circulation, 2003, vol. 34, no. 3, pp. 610-615

http://europepmc.org/abstract/med/12624280

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March 2003
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Smooth muscle cells in transplant atherosclerotic lesions are originated from recipients, but not bone marrow progenitor cells.

Hu Y, Davison F, Ludewig B, Erdel M, Mayr M, Url M, Dietrich H, Xu Q, Circulation, 2002, vol. 106, no. 14, pp. 1834-1839

http://europepmc.org/abstract/med/12356638

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October 2002
1 Read

Both donor and recipient origins of smooth muscle cells in vein graft atherosclerotic lesions

Circulation Research

Smooth muscle cell (SMC) accumulation in the inner layer of the vessel wall is a key event in the pathogenesis of atherosclerosis in vein grafts, but the origin of the cells in these lesions has yet to be shown. Herein, we use animal models of vein grafts in transgenic mice to clearly identify the sources of SMCs in atherosclerosis. Vena cava segments were isografted to carotid arteries between four types of transgenic mice, including SM-LacZ expressing beta-galactosidase (beta-gal) in vascular SMCs, SM-LacZ/apoE(-/-), ROSA26 expressing beta-gal in all tissues, and wild-type mice beta-gal-positive cells were observed in neointimal and atherosclerotic lesions of all vein segments grafted between LacZ transgenic and wild-type mice. Double staining for beta-gal and cell nuclei revealed that about 40% of SMCs originated from hosts and 60% from the donor vessel. This was confirmed by double labeling of the Y-chromosome and alpha-actin in the lesions of sex-mismatched vein grafts. The possibility that bone marrow cells were the source of SMCs in grafts was eliminated by the absence of beta-gal staining in atherosclerotic lesions of chimeric mice. Furthermore, vein SMCs of SM-LacZ mice did not express beta -gal in situ, but did so when these cells appeared in atherosclerotic lesions in vivo, suggesting that hemodynamic forces may be crucial for SMC differentiation. Thus, we provide the first evidence of SMC origins in the atherosclerotic lesions of vein grafts, which will be essential for providing insight into new types of therapy for the disease. The full text of this article is available at http://www.circresaha.org

https://kclpure.kcl.ac.uk/portal/en/publications/both-donor-and-recipient-origins-of-smooth-muscle-cells-in-vein-graft-atherosclerotic-lesions(c0e49959-d9e5-4501-9335-1cf26c6bc0de).html

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October 2002
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Mechanical stress-induced DNA damage and rac-p38MAPK signal pathways mediate p53-dependent apoptosis in vascular smooth muscle cells

Faseb Journal

Recently, we demonstrated that biomechanical stress induces apoptosis of vascular smooth muscle cells (SMCs) (Mayr et al., FASEB J. 2000; 15:261-270). In this article we investigated the molecular mechanisms of mechanical stress-induced apoptosis. When SMCs were subjected to cyclic strain, tumor-suppressor p53 was activated as evidenced by gel mobility shift assays and Western blot analyses. p53 activation was largely attenuated if SMCs were pretreated with SB202190, a specific p38MAPK inhibitor, or were stably transfected with dominant negative rac, an upstream signal transducer of p38MAPK pathways. Kinase assays provided direct evidence that p38MAPKs phosphorylated p53 within 30 min of cyclic strain. Additionally, mechanical stress resulted in oxidative DNA damage as detected by the presence of 8-oxoguanine. Treatment with the antioxidant U-74389G abrogated p53 activation. p53 activation was followed by expression and mitochondrial translocation of the proapoptotic protein Bax. Likewise, mechanical stress resulted in up-regulation of anti-apoptotic Bcl-2 proteins, including Bcl-2 and Bcl-xL. However, a marked loss of mitochondrial membrane potential occurred in wild-type, but not in p53-/-, SMCs. The latter lost their ability to express Bax and showed no apoptosis in response to cyclic strain. Taken together, our data provide the first evidence that SMC apoptosis induced by mechanical stress is p53-dependent.

https://kclpure.kcl.ac.uk/portal/en/publications/mechanical-stressinduced-dna-damage-and-racp38mapk-signal-pathways-mediate-p53dependent-apoptosis-in-vascular-smooth-muscle-cells(b878d502-4a75-4c89-9942-0efbb07cfe4f).html

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October 2002
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Active and passive smoking, chronic infections, and the risk of carotid atherosclerosis: prospective results from the Bruneck Study.

Kiechl S, Werner P, Egger G, Oberhollenzer F, Mayr M, Xu Q, Poewe W, Willeit J, Stroke; a journal of cerebral circulation, 2002, vol. 33, no. 9, pp. 2170-2176

http://europepmc.org/abstract/med/12215582

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October 2002
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Mechanical stress-induced DNA damage and rac-p38MAPK signal pathways mediate p53-dependent apoptosis in vascular smooth muscle cells.

FASEB J 2002 Sep 1;16(11):1423-5. Epub 2002 Jul 1.

Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck, Austria.

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http://www.fasebj.org/doi/10.1096/fj.02-0042fje
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http://dx.doi.org/10.1096/fj.02-0042fjeDOI Listing
September 2002
5 Reads
33 Citations
5.040 Impact Factor

Loss of p53 accelerates neointimal lesions of vein bypass grafts in mice.

Mayr U, Mayr M, Li C, Wernig F, Dietrich H, Hu Y, Xu Q, Circulation research, 2002, vol. 90, no. 2, pp. 197-204

http://europepmc.org/abstract/med/11834713

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March 2002
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Exacerbated vein graft arteriosclerosis in protein kinase Cdelta-null mice.

Leitges M, Mayr M, Braun U, Mayr U, Li C, Pfister G, Ghaffari-Tabrizi N, Baier G, Hu Y, Xu Q, The Journal of clinical investigation, 2001, vol. 108, no. 10, pp. 1505-1512

http://europepmc.org/abstract/med/11714742

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December 2001

Smooth muscle cell apoptosis in arteriosclerosis.

Authors:
Mayr M Xu Q

Mayr M, Xu Q, Experimental gerontology, 2001, vol. 36, no. 7, pp. 969-987

http://europepmc.org/abstract/med/11404045

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July 2001
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Chronic infections and the risk of carotid atherosclerosis - Prospective results from a large population study

Circulation (Baltimore)

Background-Chronic infections have been implicated in the pathogenesis of atherosclerosis, yet from an epidemiological perspective, this concept remains controversial. Methods and Results-The Bruneck Study is a prospective population-based survey on the pathogenesis of atherosclerosis, In 826 men and women 40 to 79 years old (1990 baseline), 5-year changes in carotid atherosclerosis were thoroughly assessed by high-resolution duplex scanning. The presence of chronic respiratory, urinary tract, dental, and other infections was ascertained by standard diagnostic criteria. Chronic infections amplified the risk of atherosclerosis development in the carotid arteries. The association was most pronounced in subjects free of carotid atherosclerosis at baseline (age-/sex-adjusted odds ratio [95% CI] for any chronic infection versus none, 4.08 [2.42 to 6.85]; P

https://kclpure.kcl.ac.uk/portal/en/publications/chronic-infections-and-the-risk-of-carotid-atherosclerosis--prospective-results-from-a-large-population-study(379600ac-03d4-487e-9164-6158235a4d95).html

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February 2001

Rapid development of vein graft atheroma in ApoE-deficient mice.

Dietrich H, Hu Y, Zou Y, Huemer U, Metzler B, Li C, Mayr M, Xu Q, The American journal of pathology, 2000, vol. 157, no. 2, pp. 659-669

http://europepmc.org/abstract/med/10934168

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August 2000
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Serum soluble heat shock protein 60 is elevated in subjects with atherosclerosis in a general population.

Xu Q, Schett G, Perschinka H, Mayr M, Egger G, Oberhollenzer F, Willeit J, Kiechl S, Wick G, Circulation, 2000, vol. 102, no. 1, pp. 14-20

http://europepmc.org/abstract/med/10880409

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July 2000
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Reduced neointima hyperplasia of vein bypass grafts in intercellular adhesion molecule-1-deficient mice.

Zou Y, Hu Y, Mayr M, Dietrich H, Wick G, Xu Q, Circulation research, 2000, vol. 86, no. 4, pp. 434-440

http://europepmc.org/abstract/med/10700448

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March 2000

Biomechanical stress-induced apoptosis in vein grafts involves p38 mitogen-activated protein kinases.

FASEB J 2000 Feb;14(2):261-70

Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck, Austria.

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February 2000
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27 Citations
5.040 Impact Factor

Atherogenic effects of chronic infections: the role of heat shock protein 60 in autoimmunity.

Authors:
M Mayr Q Xu G Wick

Isr Med Assoc J 1999 Dec;1(4):272-7

Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck, Austria.

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December 1999
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4 Citations

Inhibition of arteriosclerosis by T-cell depletion in normocholesterolemic rabbits immunized with heat shock protein 65.

Metzler B, Mayr M, Dietrich H, Singh M, Wiebe E, Xu Q, Wick G, Arteriosclerosis, thrombosis, and vascular biology, 1999, vol. 19, no. 8, pp. 1905-1911

http://europepmc.org/abstract/med/10446069

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August 1999
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Atherosclerosis, autoimmunity, and vascular-associated lymphoid tissue.

FASEB J 1997 Nov;11(13):1199-207

Institute of Biomedical Aging Research of the Austrian Academy of Sciences, Innsbruck.

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November 1997
2 Reads
35 Citations
5.040 Impact Factor

Macrophage-lysis mediated by autoantibodies to heat shock protein 65/60.

Schett G, Metzler B, Mayr M, Amberger A, Niederwieser D, Gupta RS, Mizzen L, Xu Q, Wick G, Atherosclerosis, 1997, vol. 128, no. 1, pp. 27-38

http://europepmc.org/abstract/med/9051195

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January 1997
1 Read

Top co-authors

Xiaoke Yin
Xiaoke Yin

King's College London

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Anna Zampetaki
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King's College London

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Stefan Kiechl
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Medical University of Innsbruck

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Peter Willeit
Peter Willeit

University of Cambridge

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Sarah R Langley
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King's College London

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Medical University of Innsbruck

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Institute of Molecular and Translational Therapeutic Strategies (IMTTS)

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Anchored Signaling

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Bruneck Hospital

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