11,172 results match your criteria Cardiovascular research[Journal]


Additive Protective Effects of Sacubitril/Valsartan and Bosentan on Vascular Remodeling in Experimental Pulmonary Hypertension.

Cardiovasc Res 2020 Jul 11. Epub 2020 Jul 11.

INSERM UMR_S 999 «Pulmonary Hypertension: Pathophysiology and Novel Therapies», Hôpital Marie Lannelongue, 92350 Le Plessis-Robinson, France.

Aims: Although right ventricular (RV) function is an important determinant of morbidity and mortality in patients with pulmonary arterial hypertension (PAH), there is no treatment targeting directly the RV. We therefore evaluate the efficacy of sacubitril/valsartan (LCZ 696) as add-on therapy to bosentan in rats with severe pulmonary hypertension (PH).

Methods And Results: Combination therapy of LCZ 696 and bosentan has additive vascular protective effects against the pulmonary vascular remodeling and PH in two preclinical models of severe PH. Read More

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http://dx.doi.org/10.1093/cvr/cvaa200DOI Listing

Diet-induced dyslipidemia induces metabolic and migratory adaptations in regulatory T cells.

Cardiovasc Res 2020 Jul 11. Epub 2020 Jul 11.

Division of BioTherapeutics, LACDR, Leiden University, Leiden, The Netherlands.

Aims: A hallmark of advanced atherosclerosis is inadequate immunosuppression by regulatory T (Treg) cells inside atherosclerotic lesions. Dyslipidemia has been suggested to alter Treg cell migration by affecting the expression of specific membrane proteins, thereby decreasing Treg cell migration towards atherosclerotic lesions. Besides membrane proteins, cellular metabolism has been shown to be a crucial factor in Treg cell migration. Read More

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http://dx.doi.org/10.1093/cvr/cvaa208DOI Listing

VE-PTP inhibition elicits eNOS phosphorylation to blunt endothelial dysfunction and hypertension in diabetes.

Cardiovasc Res 2020 Jul 11. Epub 2020 Jul 11.

Institute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Frankfurt am Main, Germany.

Aims: Receptor-type vascular endothelial protein tyrosine phosphatase (VE-PTP) dephosphorylates Tie-2 as well as CD31, VE-cadherin and VEGFR2. The latter form a signal transduction complex that mediates the endothelial cell response to shear stress, including the activation of the endothelial nitric oxide (NO) synthase (eNOS). As VE-PTP expression is increased in diabetes, we investigated the consequences of VE-PTP inhibition (using AKB-9778) on blood pressure in diabetic patients and the role of VE-PTP in the regulation of eNOS activity and vascular reactivity. Read More

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http://dx.doi.org/10.1093/cvr/cvaa213DOI Listing

Interleukin-7 and interleukin-15 drive CD4+CD28null T lymphocyte expansion and function in patients with acute coronary syndrome.

Cardiovasc Res 2020 Jul 9. Epub 2020 Jul 9.

Molecular and Clinical Sciences Research Institute, St. George's, University of London, London, UK.

Aims: Inflammation has important roles in atherosclerosis. CD4+CD28null (CD28null) T cells are a specialised T lymphocyte subset that produce inflammatory cytokines and cytotoxic molecules. CD28null T cells expand preferentially in patients with acute coronary syndrome (ACS) rather than stable angina and are barely detectable in healthy subjects. Read More

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http://dx.doi.org/10.1093/cvr/cvaa202DOI Listing

β-Adrenergic Receptors in Cardiac Muscle - it Takes Two to Tango.

Authors:
Ernst Niggli

Cardiovasc Res 2020 Jul 9. Epub 2020 Jul 9.

Department of Physiology, University of Bern, Buehlplatz 5, 3012 Bern, Switzerland.

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http://dx.doi.org/10.1093/cvr/cvaa183DOI Listing

The Glycocalyx core protein Glypican 1 protects vessel wall endothelial cells from stiffness-mediated dysfunction and disease.

Cardiovasc Res 2020 Jul 9. Epub 2020 Jul 9.

Department of Biomedical Engineering, The City College of New York, New York, NY, USA.

Aims: Arterial stiffness is an underlying risk factor and a hallmark of cardiovascular diseases. The endothelial cell (EC) glycocalyx is a glycan rich surface layer that plays a key role in protecting against EC dysfunction and vascular disease. However, the mechanisms by which arterial stiffness promotes endothelial cell dysfunction and vascular disease are not fully understood, and whether the mechanism involves the protective endothelial glycocalyx is yet to be determined. Read More

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http://dx.doi.org/10.1093/cvr/cvaa201DOI Listing

Disruption of Actin Dynamics Regulated by Rho Effector mDia1 Attenuates Pressure Overload-Induced Cardiac Hypertrophic Responses and Exacerbates Dysfunction.

Cardiovasc Res 2020 Jul 9. Epub 2020 Jul 9.

Department of Pharmacology, Oita University, Faculty of Medicine, 1-1 Idaigaoka, Hasama, Yufu, Oita, Japan.

Aims: Cardiac hypertrophy is a compensatory response to pressure overload, leading to heart failure. Recent studies have demonstrated that Rho is immediately activated in left ventricles after pressure overload, and that Rho signalling plays crucial regulatory roles in actin cytoskeleton rearrangement during cardiac hypertrophic responses. However, the mechanisms by which Rho and its downstream proteins control actin dynamics during hypertrophic responses remain not fully understood. Read More

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http://dx.doi.org/10.1093/cvr/cvaa206DOI Listing

Cardiovascular and immunological implications of social distancing in the context of COVID-19.

Cardiovasc Res 2020 Jul 8. Epub 2020 Jul 8.

William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.

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http://dx.doi.org/10.1093/cvr/cvaa167DOI Listing

Non-coding RNAs - Update on mechanisms and therapeutic targets from the ESC Working Groups of Myocardial Function and Cellular Biology of the Heart.

Cardiovasc Res 2020 Jul 8. Epub 2020 Jul 8.

Institute for Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hannover, Germany.

Vast parts of mammalian genomes are actively transcribed, predominantely giving rise to non-coding RNA transcripts including microRNAs, long non-coding RNA and circular RNAs amongst others. Contrary to previous opinions that most of these RNA are non-functional molecules, they are now recognised as critical regulators of many physiological and pathological processes including those of the cardiovascular system. The discovery of functional non-coding RNAs has opened up new research avenues aiming at understanding non-coding RNA-related disease mechanisms as well as exploiting them as novel therapeutics in cardiovascular therapy. Read More

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http://dx.doi.org/10.1093/cvr/cvaa195DOI Listing

Single-cell analysis of SARS-CoV-2 receptor ACE2 and spike protein priming expression of proteases in the human heart.

Cardiovasc Res 2020 Jul 8. Epub 2020 Jul 8.

National Clinical Research Center of Cardiovascular Diseases, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PR China.

Aims: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) directly binds to ACE2 (angiotensin-converting enzyme 2) to facilitate cellular entry. Compared with the lung or respiratory tract, the human heart exhibits greater ACE2 expression. However, little substantial damage was found in the heart tissue, and no viral particles were observed in the cardiac myocytes. Read More

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http://dx.doi.org/10.1093/cvr/cvaa191DOI Listing

Risk factors for myocardial injury and death in patients with COVID-19: insights from a cohort study with chest computed tomography.

Cardiovasc Res 2020 Jul 8. Epub 2020 Jul 8.

Department of Cardiovascular Medicine, Humanitas Clinical and Research Center, IRCCS, via Manzoni 56, 20089 Rozzano (Milan), Italy.

Aims: Whether pulmonary artery (PA) dimension and coronary artery calcium (CAC) score, as assessed by chest computed tomography (CT), are associated with myocardial injury in patients with coronavirus disease 2019 (COVID-19) is not known. The aim of this study was to explore the risk factors for myocardial injury and death and to investigate whether myocardial injury has an independent association with all-cause mortality in patients with COVID-19.

Methods And Results: This is a single-centre cohort study including consecutive patients with laboratory-confirmed COVID-19 undergoing chest CT on admission. Read More

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http://dx.doi.org/10.1093/cvr/cvaa193DOI Listing

Lose the helpers… Get 'remote' regulators!

Cardiovasc Res 2020 Jul 8. Epub 2020 Jul 8.

Experimental Vascular Biology Division, Dept. of Medical Biochemistry, University of Amsterdam, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centers, Amsterdam, The Netherlands.

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http://dx.doi.org/10.1093/cvr/cvaa197DOI Listing

Protection from cardiotoxicity of cancer chemotherapy - a novel target for remote ischaemic conditioning?

Cardiovasc Res 2020 Jul 8. Epub 2020 Jul 8.

Department of Cardiology and Vascular Medicine, West German Heart and Vascular Center, University of Essen Medical School, Essen, Germany.

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http://dx.doi.org/10.1093/cvr/cvaa199DOI Listing

Tackling myocardial oxidative stress with empagliflozin: Are we big enough to fight HFpEF?

Cardiovasc Res 2020 Jul 8. Epub 2020 Jul 8.

Center for Molecular Cardiology, University of Zürich, Wagistrasse 12, Schlieren CH-8952, Switzerland.

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http://dx.doi.org/10.1093/cvr/cvaa196DOI Listing

Genetic background of atrial fibrillation: influence of single-nucleotide polymorphisms.

Cardiovasc Res 2020 Jul;116(9):e106-e108

Institute for Experimental Cardiovascular Medicine, University Heart Center Freiburg-Bad Krozingen, Medical Center-University of Freiburg, Freiburg, Germany.

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http://dx.doi.org/10.1093/cvr/cvaa166DOI Listing

T Cell Aging in Hypertension.

Cardiovasc Res 2020 Jul 1. Epub 2020 Jul 1.

From the School of Medicine, Stanford University, Stanford, CA.

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http://dx.doi.org/10.1093/cvr/cvaa185DOI Listing

Effect of Icosapent Ethyl on Progression of Coronary Atherosclerosis in Patients with Elevated Triglycerides on Statin Therapy: A prospective, placebo-controlled randomized trial (EVAPORATE): Interim Results.

Cardiovasc Res 2020 Jul 1. Epub 2020 Jul 1.

California Cardiovascular Institute, Fresno CA.

Aims: Though statin therapy is known to slow coronary atherosclerosis progression and reduce cardiovascular(CV) events, significant CV risk still remains. In the REDUCE-IT study, icosapent ethyl (IPE) added to statin therapy reduced initial CV events by 25% and total CV events by 30%, but its effects on coronary atherosclerosis progression have not yet been fully investigated. Therefore, this study is to determine whether IPE 4g/d will result in a greater change from baseline in plaque volume measured by serial multidetector computed tomography (MDCT) than placebo in statin-treated patients. Read More

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http://dx.doi.org/10.1093/cvr/cvaa184DOI Listing

CLASS SWITCHING AND HIGH AFFINITY IgG PRODUCTION BY B CELLS IS DISPENSABLE FOR THE DEVELOPMENT OF HYPERTENSION IN MICE.

Cardiovasc Res 2020 Jul 1. Epub 2020 Jul 1.

Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA.

Aims: Elevated serum immunoglobulins have been associated with experimental and human hypertension for decades but whether immunoglobulins and B cells play a causal role in hypertension pathology is unclear. In this study, we sought to determine the role of B cells and high-affinity class-switched immunoglobulins on hypertension and hypertensive end-organ damage to determine if they might represent viable therapeutic targets for this disease.

Methods And Results: We purified serum IgG from mice exposed to vehicle or angiotensin (Ang) II to induce hypertension and adoptively transferred these to wild type (WT) recipient mice receiving a subpressor dose of Ang II. Read More

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http://dx.doi.org/10.1093/cvr/cvaa187DOI Listing

Remote Ischemic Preconditioning Ameliorates Anthracycline-induced Cardiotoxicity and Preserves Mitochondrial Integrity.

Cardiovasc Res 2020 Jun 29. Epub 2020 Jun 29.

Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.

Aims: Anthracycline-induced cardiotoxicity (AIC) is a serious adverse effect among cancer patients. A central mechanism of AIC is irreversible mitochondrial damage. Despite major efforts, there are currently no effective therapies able to prevent AIC. Read More

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http://dx.doi.org/10.1093/cvr/cvaa181DOI Listing

Single-cell RNA sequencing reveals cell type- and artery-specific vascular remodeling in male spontaneously hypertensive rats.

Cardiovasc Res 2020 Jun 26. Epub 2020 Jun 26.

School of Cardiovascular Medicine and Sciences, King's College London BHF Centre, London, UK.

Aims: Hypertension is a major risk factor for cardiovascular diseases. However, vascular remodeling, a hallmark of hypertension, has not been systematically characterized yet. We described systematic vascular remodeling, especially the artery type- and cell type-specific changes, in hypertension using spontaneously hypertensive rats. Read More

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http://dx.doi.org/10.1093/cvr/cvaa164DOI Listing

'Social distancing' of the neuronal nitric oxide synthase from its adaptor protein causes arrhythmogenic trigger-substrate interactions in Long QT Syndrome.

Cardiovasc Res 2020 Jun 26. Epub 2020 Jun 26.

Department of Internal Medicine, Section of Cardiovascular Medicine, Yale New Haven Hospital.

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http://dx.doi.org/10.1093/cvr/cvaa179DOI Listing

Tissue-selective endothelial arousal revealed by VEGF gene transfer.

Cardiovasc Res 2020 Jun 25. Epub 2020 Jun 25.

Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.

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http://dx.doi.org/10.1093/cvr/cvaa172DOI Listing

I'm pickin' up good dilations.

Authors:
Friedrich C Luft

Cardiovasc Res 2020 Jun 25. Epub 2020 Jun 25.

Experimental and Clinical Research Center, a cooperation between the Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.

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http://dx.doi.org/10.1093/cvr/cvaa177DOI Listing

The swan song of dying cells.

Cardiovasc Res 2020 Jul;116(8):e90-e92

Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, 126 University Place, University of Glasgow, Glasgow G12 8TA, UK.

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http://dx.doi.org/10.1093/cvr/cvaa152DOI Listing

Duration of antiplatelet therapy after complex PCI in the TWILIGHT-COMPLEX trial: the Goldilocks dilemma.

Cardiovasc Res 2020 Jul;116(8):e93-e95

Mount Sinai School of Medicine, New York, NY, USA.

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http://dx.doi.org/10.1093/cvr/cvaa135DOI Listing

Zoom-ing towards the Frontiers of science: a report on the first virtual session from Cardiovascular Research.

Cardiovasc Res 2020 Jul;116(8):e103-e105

BHF Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.

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http://dx.doi.org/10.1093/cvr/cvaa138DOI Listing

Inappropriate evaluation of methodology and biases by P. Morfeld and T.C. Erren.

Cardiovasc Res 2020 Jul;116(8):e102

University Medical Center of the Johannes Gutenberg University, Mainz, Germany.

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http://dx.doi.org/10.1093/cvr/cvaa130DOI Listing

Melatonin: shining some light on pulmonary hypertension.

Authors:
Margaret MacLean

Cardiovasc Res 2020 Jun 24. Epub 2020 Jun 24.

University of Strathclyde, 161, Cathedral Street, HW406, Glasgow, Dumbartonshire, G4 0RE, UK.

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http://dx.doi.org/10.1093/cvr/cvaa173DOI Listing

STANDARDIZING TRANSLATIONAL MICROBIOME STUDIES AND METAGENOMIC ANALYSES.

Cardiovasc Res 2020 Jun 22. Epub 2020 Jun 22.

Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, Wilf Family Cardiovascular Research Institute, New York, NY, USA.

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http://dx.doi.org/10.1093/cvr/cvaa175DOI Listing

Corrigendum.

Authors:

Cardiovasc Res 2020 Jun 17. Epub 2020 Jun 17.

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http://dx.doi.org/10.1093/cvr/cvaa157DOI Listing

Corrigendum.

Authors:

Cardiovasc Res 2020 Jun 17. Epub 2020 Jun 17.

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http://dx.doi.org/10.1093/cvr/cvaa153DOI Listing

Influenza-associated cardiac injury: A disease of the cardiac conduction system?

Cardiovasc Res 2020 Jun 18. Epub 2020 Jun 18.

William Harvey Research Institute, Queen Mary University of London, London, UK.

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http://dx.doi.org/10.1093/cvr/cvaa174DOI Listing
June 2020
5.940 Impact Factor

Long term dual antithrombotic therapy (DAT) - Is it efficient and safe in women?

Authors:
Meinrad Gawaz

Cardiovasc Res 2020 Jun 16. Epub 2020 Jun 16.

Department of Cardiology and Angiology, University Hospital Tübingen, Eberhard Karls University Tübingen, Tübingen, Germany.

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http://dx.doi.org/10.1093/cvr/cvaa169DOI Listing

ENDOTHELIUM-RESTRICTED ENDOTHELIN-1 OVEREXPRESSION IN TYPE-1 DIABETES WORSENS ATHEROSCLEROSIS AND IMMUNE CELL INFILTRATION VIA NOX1.

Cardiovasc Res 2020 Jun 13. Epub 2020 Jun 13.

Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research.

Aims: NADPH oxidase (NOX) 1 but not NOX4-dependent oxidative stress plays a role in diabetic vascular disease, including atherosclerosis. Endothelin (ET)-1 has been implicated in diabetes-induced vascular complications. We showed that crossing mice overexpressing human ET-1 selectively in endothelium (eET-1) with apolipoprotein E knockout (Apoe-/-) mice enhanced high-fat diet-induced atherosclerosis in part by increasing oxidative stress. Read More

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http://dx.doi.org/10.1093/cvr/cvaa168DOI Listing

Estrogen receptors and T cells determine how sex affects aldosterone-induced hypertension.

Cardiovasc Res 2020 Jun 13. Epub 2020 Jun 13.

Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research, and Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital, McGill University, 3755 Côte-Ste-Catherine Rd., Montreal, Quebec, Canada H3T 1E2.

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http://dx.doi.org/10.1093/cvr/cvaa170DOI Listing

Therapeutic potential of adenosine kinase inhibition in vascular disease.

Cardiovasc Res 2020 Jun 12. Epub 2020 Jun 12.

Biosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, International Centre for Life, Central Parkway, Newcastle Upon Tyne NE1 3BZ, UK.

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http://dx.doi.org/10.1093/cvr/cvaa122DOI Listing

Rare Loss-of-function Mutations of PTGIR are enriched in Fibromuscular Dysplasia.

Cardiovasc Res 2020 Jun 12. Epub 2020 Jun 12.

Université de Paris, Inserm UMR 970, Paris Centre de Recherche Cardiovasculaire, France.

Aims: Fibromuscular dysplasia (FMD) and spontaneous coronary artery dissection (SCAD) are related, non-atherosclerotic arterial diseases mainly affecting middle-aged women. Little is known about their physiopathological mechanisms. We aimed to identify rare genetic causes to elucidate molecular mechanisms implicated in FMD and SCAD. Read More

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http://dx.doi.org/10.1093/cvr/cvaa161DOI Listing

Stretch-induced sarcoplasmic reticulum calcium leak is causatively associated with atrial fibrillation in pressure-overloaded hearts.

Cardiovasc Res 2020 Jun 12. Epub 2020 Jun 12.

The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.

Aims: Despite numerous reports documenting an important role of hypertension in the development of atrial fibrillation (AF), the detailed mechanism underlying the pathological process remains incompletely understood. Here, we aim to test the hypothesis that diastolic sarcoplasmic reticulum (SR) Ca2+ leak in atrial myocytes, induced by mechanical stretch due to elevated pressure in the left atrium (LA), plays an essential role in the AF development in pressure-overloaded hearts.

Methods And Results: Isolated mouse atrial myocytes subjected to acute axial stretch displayed an immediate elevation of SR Ca2+ leak. Read More

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http://dx.doi.org/10.1093/cvr/cvaa163DOI Listing
June 2020
5.940 Impact Factor

Altered Atrial Cytosolic Calcium Handling Contributes to the Development of Postoperative Atrial Fibrillation.

Cardiovasc Res 2020 Jun 10. Epub 2020 Jun 10.

Institute of Pharmacology and Toxicology, University Medical Center Göttingen, Germany.

Aims: Atrial fibrillation is a commonly occurring arrhythmia after cardiac surgery (postoperative AF, poAF) and is associated with poorer outcomes. Considering that reduced atrial contractile function is a predictor of poAF and that Ca2+ plays an important role in both excitation-contraction coupling and atrial arrhythmogenesis, this study aims to test whether alterations of intracellular Ca2+ handling contribute to impaired atrial contractility and to the arrhythmogenic substrate predisposing patients to poAF.

Methods And Results: Right atrial appendages were obtained from patients in sinus rhythm undergoing open-heart surgery. Read More

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http://dx.doi.org/10.1093/cvr/cvaa162DOI Listing

Dilated Cardiomyopathy (DCM)-linked Heat shock protein Family D Member 1 (HSPD1) mutations cause upregulation of ROS and autophagy through mitochondrial dysfunction.

Cardiovasc Res 2020 Jun 10. Epub 2020 Jun 10.

Department of Cardiology; Keio University School of Medicine, Tokyo, Japan.

Background: During heart failure, the levels of circulatory HSPD1 (HSP60) increase. However, its underlying mechanism is still unknown. The apical domain of HSPD1 is conserved throughout evolution. Read More

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http://dx.doi.org/10.1093/cvr/cvaa158DOI Listing

Gender balance at the heart of science.

Cardiovasc Res 2020 Jun 9. Epub 2020 Jun 9.

Division of Paediatric Cardiology, Department of Paediatrics, Red Cross War Memorial Children's Hospital, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.

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http://dx.doi.org/10.1093/cvr/cvaa114DOI Listing

The long and winding road of cardiomyocyte maturation.

Cardiovasc Res 2020 Jun 8. Epub 2020 Jun 8.

Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Knowledge about the molecular mechanisms regulating cardiomyocyte (CM) proliferation and differentiation has increased exponentially in recent years. Such insights together with the availability of more efficient protocols for generation of CMs from induced pluripotent stem cells (iPSCs) have raised expectations for new therapeutic strategies to treat congenital and non-congenital heart diseases. However, the poor regenerative potential of the postnatal heart and the incomplete maturation of iPSC-derived CMs represent important bottlenecks for such therapies in future years. Read More

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http://dx.doi.org/10.1093/cvr/cvaa159DOI Listing

Improving Translational Research in Sex-specific Effects of Comorbidities and Risk Factors in Ischemic Heart Disease and Cardioprotection: Position Paper and Recommendations of the ESC Working Group on Cellular Biology of the Heart.

Cardiovasc Res 2020 Jun 2. Epub 2020 Jun 2.

Department of Medical Biology, UiT The Arctic University of Norway, Norway.

Ischemic heart disease (IHD) is a complex disorder and a leading cause of death and morbidity in both men and women. Sex however affects several aspects of IHD, including pathophysiology, incidence, clinical presentation, diagnosis as well as treatment and outcome. Several diseases or risk factors frequently associated with IHD can modify cellular signalling cascades, thus affecting ischemia/reperfusion injury as well as responses to cardioprotective interventions. Read More

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http://dx.doi.org/10.1093/cvr/cvaa155DOI Listing

Corrigendum.

Authors:

Cardiovasc Res 2020 Jul;116(8):1539

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http://dx.doi.org/10.1093/cvr/cvaa111DOI Listing

Corrigendum.

Authors:

Cardiovasc Res 2020 Jul;116(8):1541

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http://dx.doi.org/10.1093/cvr/cvaa112DOI Listing

Decreased myocardial infarction admissions during COVID times: what can we learn?

Cardiovasc Res 2020 May 28. Epub 2020 May 28.

Department of Cardiovascular Medicine, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.

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http://dx.doi.org/10.1093/cvr/cvaa146DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7314183PMC

Neuroimmune interactions in cardiovascular diseases.

Cardiovasc Res 2020 May 27. Epub 2020 May 27.

Department of Angiocardioneurology and Translational Medicine, IRCCS Neuromed, Pozzilli (IS), Italy.

Our body is continuously in contact with external stimuli that need a fine integration with the internal milieu in order to maintain the homeostasis. Similarly, perturbations of the internal environment are responsible for the alterations of the physiological mechanisms regulating our main functions. The nervous system and the immune system represent the main interfaces between the internal and the external environment. Read More

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http://dx.doi.org/10.1093/cvr/cvaa151DOI Listing