4,117 results match your criteria Basic research in cardiology[Journal]


The different response of cardiomyocytes and cardiac fibroblasts to mitochondria inhibition and the underlying role of STAT3.

Basic Res Cardiol 2019 Feb 14;114(2):12. Epub 2019 Feb 14.

Department of Pharmacology (the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Baojian Road 157, Harbin, 150086, People's Republic of China.

Cardiomyocyte loss and cardiac fibrosis are the main characteristics of cardiac ischemia and heart failure, and mitochondrial function of cardiomyocytes is impaired in cardiac ischemia and heart failure, so the aim of this study is to identify fate variability of cardiomyocytes and cardiac fibroblasts with mitochondria inhibition and explore the underlying mechanism. The mitochondrial respiratory function was measured by using Oxygraph-2k high-resolution respirometry. The STAT3 expression and activity were evaluated by western blot. Read More

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http://dx.doi.org/10.1007/s00395-019-0721-6DOI Listing
February 2019
1 Read

Blocking the IL-1β signalling pathway prevents chronic viral myocarditis and cardiac remodeling.

Basic Res Cardiol 2019 Jan 23;114(2):11. Epub 2019 Jan 23.

Cardiopathology, Institute for Pathology and Neuropathology, University Hospital Tübingen, Liebermeisterstrasse 8, 72076, Tübingen, Germany.

Coxsackieviruses of group B (CVB) are well-known causes of acute and chronic myocarditis. Chronic myocarditis can evolve into dilated cardiomyopathy (DCM) characterized by fibrosis and cardiac remodeling. Interleukin-1β (IL-1β) plays a decisive role in the induction of the inflammatory response as a consequence of viral replication. Read More

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http://link.springer.com/10.1007/s00395-019-0719-0
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http://dx.doi.org/10.1007/s00395-019-0719-0DOI Listing
January 2019
6 Reads
5.414 Impact Factor

Pericardial fluid: an underrated molecular library of heart conditions and a potential vehicle for cardiac therapy.

Basic Res Cardiol 2019 Jan 18;114(2):10. Epub 2019 Jan 18.

Departamento de Cirurgia e Fisiologia, Faculdade de Medicina da Universidade do Porto, UnIC-Unidade de Investigação Cardiovascular, 4200-319, Porto, Portugal.

The remote but heart-encircling location of pericardial fluid confers this biofluid unique properties. Once past the limitation of the invasive collection, for instance, on occasion of heart surgery or pericardiocentesis, the scrutiny of pericardial fluid content can be of great interest in cardiovascular research. This liquid concentrates many heart-derived factors, thus enclosing several surrogate markers for the diagnosis or prognosis of a large spectrum of diseases either pericardial (e. Read More

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http://dx.doi.org/10.1007/s00395-019-0716-3DOI Listing
January 2019
2 Reads

Repeated cell transplantation and adjunct renal denervation in ischemic heart failure: exploring modalities for improving cell therapy efficacy.

Basic Res Cardiol 2019 Jan 17;114(2). Epub 2019 Jan 17.

Cardiovascular Center of Excellence, LSU Health Sciences Center, 533 Bolivar St., Suite 408, New Orleans, LA, 70112, USA.

Enthusiasm for cell therapy for myocardial injury has waned due to equivocal benefits in clinical trials. In an attempt to improve efficacy, we investigated repeated cell therapy and adjunct renal denervation (RDN) as strategies for augmenting cardioprotection with cardiosphere-derived cells (CDCs). We hypothesized that combining CDC post-conditioning with repeated CDC doses or delayed RDN therapy would result in superior function and remodeling. Read More

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http://dx.doi.org/10.1007/s00395-019-0718-1DOI Listing
January 2019
2 Reads

Endothelial α1AMPK modulates angiotensin II-mediated vascular inflammation and dysfunction.

Basic Res Cardiol 2019 Jan 14;114(2). Epub 2019 Jan 14.

Department of Cardiology 1, Center for Cardiology, Universitätsmedizin Mainz, 55131, Mainz, Germany.

Mice with a global deletion of α1AMPK are characterized by endothelial dysfunction and NADPH oxidase subunit 2 (NOX-2)-mediated vascular oxidative stress. However, the underlying mechanisms are incompletely understood and may involve endothelial NOX-2 upregulation or facilitated vascular infiltration of phagocytic cells. Therefore, the current study was designed to investigate the vascular effects of chronic angiotensin II (AngII) infusion in mice with an endothelial-specific α1AMPK deletion. Read More

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http://link.springer.com/10.1007/s00395-019-0717-2
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http://dx.doi.org/10.1007/s00395-019-0717-2DOI Listing
January 2019
15 Reads

Inhibition of cardiomyocyte Sprouty1 protects from cardiac ischemia-reperfusion injury.

Basic Res Cardiol 2019 Jan 11;114(2). Epub 2019 Jan 11.

Research Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, P. O. BOX 5000, 90014, Oulu, Finland.

Sprouty1 (Spry1) is a negative modulator of receptor tyrosine kinase signaling, but its role in cardiomyocyte survival has not been elucidated. The aim of this study was to investigate the potential role of cardiomyocyte Spry1 in cardiac ischemia-reperfusion (I/R) injury. Infarct areas of mouse hearts showed an increase in Spry1 protein expression, which localized to cardiomyocytes. Read More

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http://link.springer.com/10.1007/s00395-018-0713-y
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http://dx.doi.org/10.1007/s00395-018-0713-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329741PMC
January 2019
2 Reads

Fibroblast polarization over the myocardial infarction time continuum shifts roles from inflammation to angiogenesis.

Basic Res Cardiol 2019 Jan 11;114(2). Epub 2019 Jan 11.

Department of Physiology and Biophysics, Mississippi Center for Heart Research, University of Mississippi Medical Center, 2500 North State St, Jackson, MS, 39216-4505, USA.

Cardiac fibroblasts are the major producers of extracellular matrix (ECM) to form infarct scar. We hypothesized that fibroblasts undergo a spectrum of phenotype states over the course of myocardial infarction (MI) from early onset to scar formation. Fibroblasts were isolated from the infarct region of C57BL/6J male mice (3-6 months old, n = 60) at days 0 (no MI control) and 1, 3, or 7 after MI. Read More

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http://dx.doi.org/10.1007/s00395-019-0715-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329742PMC
January 2019
1 Read

Effect of pulmonary artery denervation in postcapillary pulmonary hypertension: results of a randomized controlled translational study.

Basic Res Cardiol 2019 Jan 11;114(2). Epub 2019 Jan 11.

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

There is scarce evidence for pulmonary artery denervation (PADN) as a potential treatment for chronic postcapillary pulmonary hypertension (PH). We aimed to perform a proof-of-concept of PADN in a translational model of chronic PH. Nineteen pigs with chronic postcapillary PH (secondary to pulmonary vein banding) were randomized to surgical-PADN (using bipolar radiofrequency clamps) or sham procedure. Read More

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http://dx.doi.org/10.1007/s00395-018-0714-xDOI Listing
January 2019
3 Reads

Inflammatory cells and their non-coding RNAs as targets for treating myocardial infarction.

Basic Res Cardiol 2018 Dec 6;114(1). Epub 2018 Dec 6.

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

Myocardial infarction triggers infiltration of several types of immune cells that coordinate both innate and adaptive immune responses. These play a dual role in post-infarction cardiac remodeling by initiating and resolving inflammatory processes, which needs to occur in a timely and well-orchestrated way to ensure a reestablishment of normalized cardiac functions. Thus, therapeutic modulation of immune responses might have benefits for infarct patients. Read More

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http://link.springer.com/10.1007/s00395-018-0712-z
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http://dx.doi.org/10.1007/s00395-018-0712-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6290728PMC
December 2018
7 Reads

Epigenetically modified cardiac mesenchymal stromal cells limit myocardial fibrosis and promote functional recovery in a model of chronic ischemic cardiomyopathy.

Basic Res Cardiol 2018 Nov 16;114(1). Epub 2018 Nov 16.

Institute of Molecular Cardiology, Division of Cardiovascular Medicine, University of Louisville, 580 S. Preston Street, Louisville, KY, 40292, USA.

Preclinical investigations support the concept that donor cells more oriented towards a cardiovascular phenotype favor repair. In light of this philosophy, we previously identified HDAC1 as a mediator of cardiac mesenchymal cell (CMC) cardiomyogenic lineage commitment and paracrine signaling potency in vitro-suggesting HDAC1 as a potential therapeutically exploitable target to enhance CMC cardiac reparative capacity. In the current study, we examined the effects of pharmacologic HDAC1 inhibition, using the benzamide class 1 isoform-selective HDAC inhibitor entinostat (MS-275), on CMC cardiomyogenic lineage commitment and CMC-mediated myocardial repair in vivo. Read More

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http://link.springer.com/10.1007/s00395-018-0710-1
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http://dx.doi.org/10.1007/s00395-018-0710-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6335654PMC
November 2018
29 Reads
5.414 Impact Factor

Of mice and men: models and mechanisms of diabetic cardiomyopathy.

Basic Res Cardiol 2018 Nov 15;114(1). Epub 2018 Nov 15.

Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover, 30625, Germany.

Diabetes mellitus increases the risk of heart failure independent of co-existing hypertension and coronary artery disease. Although several molecular mechanisms for the development of diabetic cardiomyopathy have been identified, they are incompletely understood. The pathomechanisms are multifactorial and as a consequence, no causative treatment exists at this time to modulate or reverse the molecular changes contributing to accelerated cardiac dysfunction in diabetic patients. Read More

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http://link.springer.com/10.1007/s00395-018-0711-0
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http://dx.doi.org/10.1007/s00395-018-0711-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6244639PMC
November 2018
9 Reads
5.414 Impact Factor

Elevated monocyte-specific type I interferon signalling correlates positively with cardiac healing in myocardial infarct patients but interferon alpha application deteriorates myocardial healing in rats.

Basic Res Cardiol 2018 Nov 12;114(1). Epub 2018 Nov 12.

Department of Cardiology, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, Amsterdam, The Netherlands.

Monocytes are involved in adverse left ventricular (LV) remodelling following myocardial infarction (MI). To provide therapeutic opportunities we aimed to identify gene transcripts in monocytes that relate to post-MI healing and evaluated intervention with the observed gene activity in a rat MI model. In 51 MI patients treated by primary percutaneous coronary intervention (PCI), the change in LV end-diastolic volume index (EDVi) from baseline to 4-month follow-up was assessed using cardiovascular magnetic resonance imaging (CMR). Read More

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http://link.springer.com/10.1007/s00395-018-0709-7
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http://dx.doi.org/10.1007/s00395-018-0709-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6244641PMC
November 2018
9 Reads

Uncoupling protein 3 deficiency impairs myocardial fatty acid oxidation and contractile recovery following ischemia/reperfusion.

Basic Res Cardiol 2018 Oct 29;113(6):47. Epub 2018 Oct 29.

Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 N. State St., Jackson, MS, 39216-4505, USA.

Patients with insulin resistance and type 2 diabetes have poor cardiac outcomes following myocardial infarction (MI). The mitochondrial uncoupling protein 3 (UCP3) is down-regulated in the heart with insulin resistance. We hypothesized that decreased UCP3 levels contribute to poor cardiac recovery following ischemia/reperfusion (I/R). Read More

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http://link.springer.com/10.1007/s00395-018-0707-9
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http://dx.doi.org/10.1007/s00395-018-0707-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6208686PMC
October 2018
12 Reads

Cardiac mesenchymal cells from diabetic mice are ineffective for cell therapy-mediated myocardial repair.

Basic Res Cardiol 2018 Oct 23;113(6):46. Epub 2018 Oct 23.

Division of Cardiovascular Medicine, Department of Medicine, Institute of Molecular Cardiology, Envirome Institute, Diabetes and Obesity Center, University of Louisville School of Medicine, 580 S. Preston St., Rm 321E, Louisville, KY, 40202, USA.

Although cell therapy improves cardiac function after myocardial infarction, highly variable results and limited understanding of the underlying mechanisms preclude its clinical translation. Because many heart failure patients are diabetic, we examined how diabetic conditions affect the characteristics of cardiac mesenchymal cells (CMC) and their ability to promote myocardial repair in mice. To examine how diabetes affects CMC function, we isolated CMCs from non-diabetic C57BL/6J (CMC) or diabetic B6. Read More

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http://dx.doi.org/10.1007/s00395-018-0703-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6314032PMC
October 2018
5 Reads

Purinergic receptor Y (P2Y)- dependent VCAM-1 expression promotes immune cell infiltration in metabolic syndrome.

Basic Res Cardiol 2018 Oct 18;113(6):45. Epub 2018 Oct 18.

Department of Cardiology and Angiology I, University Heart Center Freiburg, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106, Freiburg, Germany.

Sterile inflammation of visceral fat, provoked by dying adipocytes, links the metabolic syndrome to cardiovascular disease. Danger-associated molecular patterns, such as adenosine triphosphate (ATP), are released by activated or dying cells and orchestrate leukocyte infiltration and inflammation via the purinergic receptor P2Y. The gene expression of ATP receptor P2Y did not change in several tissues in the course of obesity, but was increased within epididymal fat. Read More

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http://link.springer.com/10.1007/s00395-018-0702-1
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http://dx.doi.org/10.1007/s00395-018-0702-1DOI Listing
October 2018
12 Reads

The role of Wnt signaling in the healing myocardium: a focus on cell specificity.

Basic Res Cardiol 2018 Oct 16;113(6):44. Epub 2018 Oct 16.

Department of Internal Medicine III, University Hospital Heidelberg, University of Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.

Various cell types are involved in the healing process after myocardial infarction (MI). Besides cardiac resident cells (such as cardiomyocytes, fibroblasts and endothelial cells) already present at the lesion site, a massive influx of leukocytes (mainly monocytes and neutrophils) is observed within hours after the ischemic event. So far, little is known about modes of interaction of these cells. Read More

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http://link.springer.com/10.1007/s00395-018-0705-y
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http://dx.doi.org/10.1007/s00395-018-0705-yDOI Listing
October 2018
11 Reads

The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection-evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology.

Basic Res Cardiol 2018 Oct 11;113(6):43. Epub 2018 Oct 11.

The Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.

Due to its poor capacity for regeneration, the heart is particularly sensitive to the loss of contractile cardiomyocytes. The onslaught of damage caused by ischaemia and reperfusion, occurring during an acute myocardial infarction and the subsequent reperfusion therapy, can wipe out upwards of a billion cardiomyocytes. A similar program of cell death can cause the irreversible loss of neurons in ischaemic stroke. Read More

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http://link.springer.com/10.1007/s00395-018-0704-z
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http://dx.doi.org/10.1007/s00395-018-0704-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6182684PMC
October 2018
21 Reads

Raf kinase inhibitor protein mediates myocardial fibrosis under conditions of enhanced myocardial oxidative stress.

Basic Res Cardiol 2018 09 6;113(6):42. Epub 2018 Sep 6.

Klinik und Poliklinik für Kardiologie, Universitätsklinikum Leipzig, Liebigstrasse 20, 04103, Leipzig, Germany.

Fibrosis is a hallmark of maladaptive cardiac remodelling. Here we report that genome-wide quantitative trait locus (QTL) analyses in recombinant inbred mouse lines of C57BL/6 J and DBA2/J strains identified Raf Kinase Inhibitor Protein (RKIP) as genetic marker of fibrosis progression. C57BL/6 N-RKIP mice demonstrated diminished fibrosis induced by transverse aortic constriction (TAC) or CCl (carbon tetrachloride) treatment compared with wild-type controls. Read More

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http://dx.doi.org/10.1007/s00395-018-0700-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6133069PMC
September 2018
12 Reads

Rat atrial engineered heart tissue: a new in vitro model to study atrial biology.

Basic Res Cardiol 2018 09 3;113(5):41. Epub 2018 Sep 3.

DZHK (German Centre for Cardiovascular Research), Partner site Hamburg/Kiel/Lübeck, Hamburg, Germany.

Engineered heart tissue (EHT) from rat cells is a useful tool to study ventricular biology and cardiac drug safety. Since atrial and ventricular cells differ significantly, EHT and other 3D cell culture formats generated from ventricular cells have been of limited value to study atrial biology. To date, reliable in vitro models that reflect atrial physiology are lacking. Read More

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http://dx.doi.org/10.1007/s00395-018-0701-2DOI Listing
September 2018
11 Reads

LXR/RXR signaling and neutrophil phenotype following myocardial infarction classify sex differences in remodeling.

Basic Res Cardiol 2018 08 21;113(5):40. Epub 2018 Aug 21.

Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216-4505, USA.

Sex differences in heart failure development following myocardial infarction (MI) are not fully understood. We hypothesized that differential MI signaling could explain variations in outcomes. Analysis of the mouse heart attack research tool 1. Read More

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http://dx.doi.org/10.1007/s00395-018-0699-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6105266PMC
August 2018
7 Reads

A novel genetic marker of decreased inflammation and improved survival after acute myocardial infarction.

Basic Res Cardiol 2018 08 10;113(5):38. Epub 2018 Aug 10.

Cardiovascular Division, Department of Medicine, Washington University School of Medicine, 660 S. Euclid Ave., Campus, Box 8086, Saint Louis, MO, 63110, USA.

The CHRNA5 gene encodes a neurotransmitter receptor subunit involved in multiple processes, including cholinergic autonomic nerve activity and inflammation. Common variants in CHRNA5 have been linked with atherosclerotic cardiovascular disease. Association of variation in CHRNA5 and specific haplotypes with cardiovascular outcomes has not been described. Read More

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http://dx.doi.org/10.1007/s00395-018-0697-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292447PMC
August 2018
7 Reads

Activating transcription factor 3 in cardiovascular diseases: a potential therapeutic target.

Basic Res Cardiol 2018 08 9;113(5):37. Epub 2018 Aug 9.

Department of Cardiology, Renmin Hospital of Wuhan University, JieFang Road 238, Wuhan, 430060, People's Republic of China.

Cardiovascular diseases (CVDs) are the primary causes of death worldwide. Among the numerous signaling molecules involved in CVDs, transcriptional factors directly influence gene expression and play a critical role in regulating cell function and the development of diseases. Activating transcription factor (ATF) 3 is an adaptive-response gene in the ATF/cAMP responsive element-binding (CREB) protein family of transcription factors that acts as either a repressor or an activator of transcription via the formation of homodimers or heterodimers with other ATF/CREB members. Read More

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http://link.springer.com/10.1007/s00395-018-0698-6
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http://dx.doi.org/10.1007/s00395-018-0698-6DOI Listing
August 2018
13 Reads
5.414 Impact Factor

Intravenous miR-144 reduces left ventricular remodeling after myocardial infarction.

Basic Res Cardiol 2018 08 6;113(5):36. Epub 2018 Aug 6.

Division of Cardiology, Labatt Family Heart Center, Hospital for Sick Children, Toronto, ON, Canada.

MicroRNA-144 is a cytoprotective miRNA. Our previous study showed that miR-144 provides potent acute cardioprotection in an ischemia/reperfusion injury model. This study was performed to further assess whether miR-144 improves post-MI remodeling in a non-reperfused myocardial infarction (MI) model. Read More

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http://dx.doi.org/10.1007/s00395-018-0694-xDOI Listing
August 2018
6 Reads

Increased cardiac sympathetic nerve activity in ovine heart failure is reduced by lesion of the area postrema, but not lamina terminalis.

Basic Res Cardiol 2018 08 3;113(5):35. Epub 2018 Aug 3.

Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, 3052, Australia.

Increased cardiac sympathetic nerve activity (CSNA) is a key feature of heart failure (HF) and is associated with poor outcome. There is evidence that central angiotensinergic mechanisms contribute to the increased CSNA in HF, but the central sites involved are unknown. In an ovine, rapid pacing model of HF, we investigated the contribution of the lamina terminalis and area postrema to the increased CSNA and also the responses to fourth ventricular infusion of the angiotensin type 1 receptor antagonist losartan. Read More

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http://dx.doi.org/10.1007/s00395-018-0695-9DOI Listing
August 2018
2 Reads

Mechanisms underlying coronary autoregulation continue to await clarification.

Authors:
Andreas Deussen

Basic Res Cardiol 2018 08 3;113(5):34. Epub 2018 Aug 3.

Department of Physiology, Medical Faculty Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307, Dresden, Germany.

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http://dx.doi.org/10.1007/s00395-018-0693-yDOI Listing
August 2018
3 Reads

Local metabolic hypothesis is not sufficient to explain coronary autoregulatory behavior.

Basic Res Cardiol 2018 08 2;113(5):33. Epub 2018 Aug 2.

Department of Cellular and Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, IN, 46202, USA.

The local metabolic hypothesis proposes that myocardial oxygen tension determines the degree of autoregulation by increasing the production of vasodilator metabolites as perfusion pressure is reduced. Thus, normal physiologic levels of coronary venous PO, an index of myocardial oxygenation, are proposed to be required for effective autoregulation. The present study challenged this hypothesis through determination of coronary responses to changes in coronary perfusion pressure (CPP 140-40 mmHg) in open-chest swine in the absence (n = 7) and presence of euvolemic hemodilution (~ 50% reduction in hematocrit), with (n = 5) and without (n = 6) infusion of dobutamine to augment MVO. Read More

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http://dx.doi.org/10.1007/s00395-018-0691-0DOI Listing
August 2018
10 Reads

Caspase-1 inhibition by VX-765 administered at reperfusion in P2Y receptor antagonist-treated rats provides long-term reduction in myocardial infarct size and preservation of ventricular function.

Basic Res Cardiol 2018 07 10;113(5):32. Epub 2018 Jul 10.

Center for Lung Biology, University of South Alabama College of Medicine, Medical Sciences Building, Mobile, AL, 36688, USA.

Patients with acute myocardial infarction receive a P2Y receptor antagonist prior to reperfusion, a treatment that has reduced, but not eliminated, mortality, or heart failure. We tested whether the caspase-1 inhibitor VX-765 given at reperfusion (a requirement for clinical use) can provide sustained reduction of infarction and long-term preservation of ventricular function in a pre-clinical model of ischemia/reperfusion that had been treated with a P2Y receptor antagonist. To address, the hypothesis open-chest rats were subjected to 60-min left coronary artery branch occlusion/120-min reperfusion. Read More

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http://dx.doi.org/10.1007/s00395-018-0692-zDOI Listing
July 2018
14 Reads

A concise discussion of the regulatory role of cGMP kinase I in cardiac physiology and pathology.

Authors:
Franz Hofmann

Basic Res Cardiol 2018 06 22;113(4):31. Epub 2018 Jun 22.

Institut für Pharmakologie und Toxikologie, TU München, Biedersteiner Str. 29, 80802, Munich, Germany.

The underlying cause of cardiac hypertrophy, fibrosis, and heart failure has been investigated in great detail using different mouse models. These studies indicated that cGMP and cGMP-dependent protein kinase type I (cGKI) may ameliorate these negative phenotypes in the adult heart. Recently, evidence has been published that cardiac mitochondrial BKCa channels are a target for cGKI and that activation of mitoBKCa channels may cause some of the positive effects of conditioning in ischemia/reperfusion injury. Read More

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http://dx.doi.org/10.1007/s00395-018-0690-1DOI Listing
June 2018
6 Reads

Apolipoprotein A-I proteolysis in aortic valve stenosis: role of cathepsin S.

Basic Res Cardiol 2018 06 18;113(4):30. Epub 2018 Jun 18.

Montreal Heart Institute, Université de Montréal, 5000 Belanger Street, Montreal, H1T 1C8, Canada.

Aortic valve stenosis (AVS) is the most common valvular heart disease in the Western world. Therapy based on apolipoprotein A-I (apoA-I), the major protein component of high-density lipoproteins, results in AVS regression in experimental models. Nevertheless, apoA-I degradation by proteases might lead to suboptimal efficacy of such therapy. Read More

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http://dx.doi.org/10.1007/s00395-018-0689-7DOI Listing
June 2018
4 Reads

Physiological and unappreciated roles of CaMKII in the heart.

Basic Res Cardiol 2018 06 15;113(4):29. Epub 2018 Jun 15.

Department for Molecular Cardiology and Epigenetics, University Hospital Heidelberg, Im Neuenheimer Feld 669, 69120, Heidelberg, Germany.

In the cardiomyocyte, CaMKII has been identified as a nodal influencer of excitation-contraction and also excitation-transcription coupling. Its activity can be regulated in response to changes in intracellular calcium content as well as after several post-translational modifications. Some of the effects mediated by CaMKII may be considered adaptive, while effects of sustained CaMKII activity may turn into the opposite and are detrimental to cardiac integrity and function. Read More

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http://dx.doi.org/10.1007/s00395-018-0688-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6003982PMC
June 2018
4 Reads

Cardiomyocyte dimethylarginine dimethylaminohydrolase1 attenuates left-ventricular remodeling after acute myocardial infarction: involvement in oxidative stress and apoptosis.

Basic Res Cardiol 2018 06 11;113(4):28. Epub 2018 Jun 11.

Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.

Asymmetric dimethylarginine (ADMA) is a risk factor for heart diseases. Dimethylarginine dimethylaminohydrolase (DDAH) enzymes are key proteins for ADMA degradation. Endothelial DDAH1 is a vital regulator of angiogenesis. Read More

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http://dx.doi.org/10.1007/s00395-018-0685-yDOI Listing
June 2018
9 Reads
5.410 Impact Factor

Atrial fibrillation and heart failure-associated remodeling of two-pore-domain potassium (K) channels in murine disease models: focus on TASK-1.

Basic Res Cardiol 2018 06 7;113(4):27. Epub 2018 Jun 7.

Department of Cardiology, University of Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.

Understanding molecular mechanisms involved in atrial tissue remodeling and arrhythmogenesis in atrial fibrillation (AF) is essential for developing specific therapeutic approaches. Two-pore-domain potassium (K) channels modulate cellular excitability, and TASK-1 (K3.1) currents were recently shown to alter atrial action potential duration in AF and heart failure (HF). Read More

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http://dx.doi.org/10.1007/s00395-018-0687-9DOI Listing
June 2018
46 Reads

Mapping macrophage polarization over the myocardial infarction time continuum.

Basic Res Cardiol 2018 06 4;113(4):26. Epub 2018 Jun 4.

Department of Physiology and Biophysics, Mississippi Center for Heart Research, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216-4505, USA.

In response to myocardial infarction (MI), cardiac macrophages regulate inflammation and scar formation. We hypothesized that macrophages undergo polarization state changes over the MI time course and assessed macrophage polarization transcriptomic signatures over the first week of MI. C57BL/6 J male mice (3-6 months old) were subjected to permanent coronary artery ligation to induce MI, and macrophages were isolated from the infarct region at days 1, 3, and 7 post-MI. Read More

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http://dx.doi.org/10.1007/s00395-018-0686-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986831PMC
June 2018
16 Reads

Neural mechanisms in remote ischaemic conditioning in the heart and brain: mechanistic and translational aspects.

Basic Res Cardiol 2018 06 1;113(4):25. Epub 2018 Jun 1.

The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.

Remote ischaemic conditioning (RIC) is a promising method of cardioprotection, with numerous clinical studies having demonstrated its ability to reduce myocardial infarct size and improve prognosis. On the other hand, there are several clinical trials, in particular those conducted in the setting of elective cardiac surgery, that have failed to show any benefit of RIC. These contradictory data indicate that there is insufficient understanding of the mechanisms underlying RIC. Read More

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http://dx.doi.org/10.1007/s00395-018-0684-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5984640PMC
June 2018
6 Reads

cGMP at the centre of attention: emerging strategies for activating the cardioprotective PKG pathway.

Basic Res Cardiol 2018 05 15;113(4):24. Epub 2018 May 15.

Experimental Medicine and Immunotherapeutics, Department of Medicine, University of Cambridge, Addenbrookes Box 110, Cambridge, CB2 0QQ, UK.

The nitric oxide (NO)-protein kinase G (PKG) pathway has been known for some time to be an important target for cardioprotection against ischaemia/reperfusion injury and heart failure. While many approaches for reducing infarct size in patients have failed in the past, the advent of novel drugs that modulate cGMP and its downstream targets shows very promising results in recent preclinical and clinical studies. Here, we review main aspects of the NO-PKG pathway in light of recent drug development and summarise potential cardioprotective strategies in which cGMP is the main player. Read More

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http://dx.doi.org/10.1007/s00395-018-0679-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5954070PMC
May 2018
3 Reads

Vagus nerve stimulation exerts cardioprotection against myocardial ischemia/reperfusion injury predominantly through its efferent vagal fibers.

Basic Res Cardiol 2018 05 9;113(4):22. Epub 2018 May 9.

Faculty of Medicine, Cardiac Electrophysiology Research and Training Center, Chiang Mai University, Chiang Mai, 50200, Thailand.

Vagus nerve stimulation (VNS) has been shown to exert cardioprotection against myocardial ischemia/reperfusion (I/R) injury. However, whether the cardioprotection of VNS is mainly due to direct activation through its ipsilateral efferent fibers (motor) rather than indirect effects mediated by the afferent fibers (sensory) have not been clearly understood. We hypothesized that VNS exerts cardioprotection predominantly through its efferent vagal fibers. Read More

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http://dx.doi.org/10.1007/s00395-018-0683-0DOI Listing
May 2018
11 Reads

NR4A1 aggravates the cardiac microvascular ischemia reperfusion injury through suppressing FUNDC1-mediated mitophagy and promoting Mff-required mitochondrial fission by CK2α.

Basic Res Cardiol 2018 05 9;113(4):23. Epub 2018 May 9.

Department of Cardiology, PLA General Hospital, Beijing, China.

Mitochondrial fission and mitophagy are considered key processes involved in the pathogenesis of cardiac microvascular ischemia reperfusion (IR) injury although the upstream regulatory mechanism for fission and mitophagy still remains unclear. Herein, we reported that NR4A1 was significantly upregulated following cardiac microvascular IR injury, and its level was positively correlated with microvascular collapse, endothelial cellular apoptosis and mitochondrial damage. However, NR4A1-knockout mice exhibited resistance against the acute microvascular injury and mitochondrial dysfunction compared with the wild-type mice. Read More

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http://dx.doi.org/10.1007/s00395-018-0682-1DOI Listing
May 2018
44 Reads
5 Citations
5.414 Impact Factor

Retraction Note to: Compensatory role of the NBCn1 sodium/bicarbonate cotransporter on Ca-induced mitochondrial swelling in hypertrophic hearts.

Basic Res Cardiol 2018 04 18;113(3):21. Epub 2018 Apr 18.

Centro de Investigaciones Cardiovasculares CIC-CONICET, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Calle 60 y 120, 1900, La Plata, Argentina.

The authors have retracted this article [1] because of modifications in the control lanes of Figs. 2a and 8a of the COX1 blot obtained for 18-week-old rats (rotation, horizontal flipping and re-use of the control lanes for the 35-week-old rats blot). In light of the concerns raised, the conclusions drawn in this article cannot be relied upon. Read More

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http://dx.doi.org/10.1007/s00395-018-0680-3DOI Listing
April 2018
5 Reads

The GTN patch: a simple and effective new approach to cardioprotection?

Basic Res Cardiol 2018 04 17;113(3):20. Epub 2018 Apr 17.

The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.

There remains a significant un-met need to reduce the extent of myocardial injury caused by ischaemia and reperfusion injury in patients experiencing an ST-elevation MI. Although nitric oxide is central to many cardioprotective strategies currently undergoing investigation, cardioprotection from the delivery of nitrates/nitrites has been inconsistently observed. The route of administration appears to be a critical variable. Read More

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http://dx.doi.org/10.1007/s00395-018-0681-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5904221PMC
April 2018
5 Reads

T-bet deficiency attenuates cardiac remodelling in rats.

Basic Res Cardiol 2018 03 21;113(3):19. Epub 2018 Mar 21.

Department of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, 430060, People's Republic of China.

Previous studies have suggested the involvement of CD4 + T lymphocytes in cardiac remodelling. T-bet can direct Th1 lineage commitment. This study aimed to investigate the functional significance of T-bet in cardiac remodelling induced by pressure overload using T-bet global knockout rats. Read More

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http://dx.doi.org/10.1007/s00395-018-0678-xDOI Listing
March 2018
9 Reads

Role of the angiotensin-converting enzyme in the G-CSF-induced mobilization of progenitor cells.

Basic Res Cardiol 2018 03 17;113(3):18. Epub 2018 Mar 17.

Institute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany.

In addition to being a peptidase, the angiotensin-converting enzyme (ACE) can be phosphorylated and involved in signal transduction. We evaluated the role of ACE in granulocyte-colony-stimulating factor (G-CSF)-induced hematopoietic progenitor cell (HPC) mobilization and detected a significant increase in mice-lacking ACE. Transplantation experiments revealed that the loss of ACE in the HPC microenvironment rather than in the HPCs increased mobilization. Read More

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http://dx.doi.org/10.1007/s00395-018-0677-yDOI Listing
March 2018
6 Reads

Editorial Expression of Concern to: Compensatory role of the NBCn1 sodium/bicarbonate cotransporter on Ca-induced mitochondrial swelling in hypertrophic hearts.

Basic Res Cardiol 2018 03 15;113(3):17. Epub 2018 Mar 15.

Centro de Investigaciones Cardiovasculares CIC-CONICET, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Calle 60 y 120, 1900, La Plata, Argentina.

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http://dx.doi.org/10.1007/s00395-018-0676-zDOI Listing
March 2018
10 Reads

Remote ischemic preconditioning fails to reduce infarct size in the Zucker fatty rat model of type-2 diabetes: role of defective humoral communication.

Basic Res Cardiol 2018 03 9;113(3):16. Epub 2018 Mar 9.

Cardiovascular Research Institute, Wayne State University School of Medicine, Scott Hall, Room 4356, 540 E Canfield, Detroit, MI, 48201, USA.

Remote ischemic preconditioning (RIPC), the phenomenon whereby brief ischemic episodes in distant tissues or organs render the heart resistant to infarction, has been exhaustively demonstrated in preclinical models. Moreover, emerging evidence suggests that exosomes play a requisite role in conveying the cardioprotective signal from remote tissue to the myocardium. However, in cohorts displaying clinically common comorbidities-in particular, type-2 diabetes-the infarct-sparing effect of RIPC may be confounded for as-yet unknown reasons. Read More

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http://dx.doi.org/10.1007/s00395-018-0674-1DOI Listing
March 2018
6 Reads

25 years of remote ischemic conditioning: from laboratory curiosity to clinical outcome.

Authors:
Gerd Heusch

Basic Res Cardiol 2018 03 7;113(3):15. Epub 2018 Mar 7.

Institute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, Essen, Germany.

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http://dx.doi.org/10.1007/s00395-018-0673-2DOI Listing
March 2018
5 Reads

Randomized controlled trial of remote ischaemic conditioning in ST-elevation myocardial infarction as adjuvant to primary angioplasty (RIC-STEMI).

Basic Res Cardiol 2018 03 7;113(3):14. Epub 2018 Mar 7.

Department of Surgery and Physiology, Cardiovascular R&D Unit, Faculty of Medicine, University of Porto, Alameda Prof. Hernâni Monteiro, 4200-319, Porto, Portugal.

To test whether remote ischaemic conditioning (RIC) as adjuvant to standard of care (SOC) would prevent progression towards heart failure (HF) after ST-elevation myocardial infarction (STEMI). Single-centre parallel 1:1 randomized trial (computerized block-randomization, concealed allocation) to assess superiority of RIC (3 cycles of intermittent 5 min lower limb ischaemia) over SOC in consecutive STEMI patients (NCT02313961, clinical trials.gov). Read More

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http://dx.doi.org/10.1007/s00395-018-0672-3DOI Listing
March 2018
5 Reads

Cardioprotective effect of ghrelin against myocardial infarction-induced left ventricular injury via inhibition of SOCS3 and activation of JAK2/STAT3 signaling.

Basic Res Cardiol 2018 02 1;113(2):13. Epub 2018 Feb 1.

Department of Basic Medical Sciences, College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, 14611, Saudi Arabia.

The molecular mechanisms through which ghrelin exerts its cardioprotective effects during cardiac remodeling post-myocardial infarction (MI) are poorly understood. The aim of this study was to investigate whether the cardioprotection mechanisms are mediated by modulation of JAK/STAT signaling and what triggers this modulation. Rats were divided into six groups (n = 12/group): control, sham, sham + ghrelin (100 µg/kg, s. Read More

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http://link.springer.com/10.1007/s00395-018-0671-4
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http://dx.doi.org/10.1007/s00395-018-0671-4DOI Listing
February 2018
17 Reads

Amphiregulin enhances cardiac fibrosis and aggravates cardiac dysfunction in mice with experimental myocardial infarction partly through activating EGFR-dependent pathway.

Basic Res Cardiol 2018 01 18;113(2):12. Epub 2018 Jan 18.

Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road, Shanghai, 200233, China.

Cardiac fibrosis (CF), a main process of ventricular remodeling after myocardial infarction (MI), plays a crucial role in the pathogenesis of heart failure (HF) post-MI. It is known that amphiregulin (AR) is involved in fibrosis of several organs. However, the expression of AR and its role post-MI are yet to be determined. Read More

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http://dx.doi.org/10.1007/s00395-018-0669-yDOI Listing
January 2018
12 Reads

Molecular imaging of cardiac remodelling after myocardial infarction.

Basic Res Cardiol 2018 01 17;113(2):10. Epub 2018 Jan 17.

School of Biomedical Engineering and Imaging Sciences, King's College London, St. Thomas Hospital, 4th Floor, Lambeth Wing, London, SE1 7EH, UK.

Myocardial infarction and subsequent heart failure is a major health burden associated with significant mortality and morbidity in western societies. The ability of cardiac tissue to recover after myocardial infarction is affected by numerous complex cellular and molecular pathways. Unbalance or failure of these pathways can lead to adverse remodelling of the heart and poor prognosis. Read More

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http://dx.doi.org/10.1007/s00395-018-0668-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5772148PMC
January 2018
11 Reads

Phosphorylation of vasodilator-stimulated phosphoprotein contributes to myocardial ischemic preconditioning.

Basic Res Cardiol 2018 01 17;113(2):11. Epub 2018 Jan 17.

Department of Anesthesiology and Intensive Care Medicine, Universitätsklinikum Tübingen, Hoppe-Seyler-Straße 3, 72076, Tübingen, Germany.

Ischemic preconditioning (IP) is a well-known strategy to protect organs against cell death following ischemia. The previous work has shown that vasodilator-stimulated phosphoprotein (VASP) is involved in cytoskeletal reorganization and that it holds significant importance for the extent of myocardial ischemia reperfusion injury. Yet, the role of VASP during myocardial IP is, to date, not known. Read More

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http://dx.doi.org/10.1007/s00395-018-0667-0DOI Listing
January 2018
5 Reads