10,474 results match your criteria Cardiovascular research[Journal]


Differential regulation of sodium channels as a novel proarrhythmic mechanism in the human failing heart.

Cardiovasc Res 2018 Jun 20. Epub 2018 Jun 20.

Clinic for Cardiology & Pneumology, Georg-August University Goettingen, and DZHK (German Centre for Cardiovascular Research), partner site Goettingen, Germany.

Aims: In heart failure, enhanced persistent Na+ current (INaL) exerts detrimental effects on cellular electrophysiology and can induce arrhythmias. However, the underlying regulatory mechanisms remain unclear. Our aim was to potentially investigate the regulation and electrophysiological contribution of neuronal sodium channel Nav1. Read More

View Article

TRPV4 increases cardiomyocyte calcium cycling and contractility yet contributes to damage in the aged heart following hypoosmotic stress.

Cardiovasc Res 2018 Jun 20. Epub 2018 Jun 20.

Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO 65212, USA.

Aims: Cardiomyocyte Ca2+ homeostasis is altered with aging via poorly-understood mechanisms. The Transient Receptor Potential Vanilloid 4 (TRPV4) ion channel is an osmotically-activated Ca2+ channel and there is limited information on the role of TRPV4 in cardiomyocytes. Our data show that TRPV4 protein expression increases in cardiomyocytes of the aged heart. Read More

View Article

Decreased mitochondrial respiration in aneurysmal aortas of Fibulin-4 mutant mice is linked to PGC1A regulation.

Cardiovasc Res 2018 Jun 21. Epub 2018 Jun 21.

Department of Vascular Surgery, Erasmus MC, Rotterdam, The Netherlands.

Aim: Thoracic aortic aneurysms are a life-threatening condition often diagnosed too late. To discover novel robust biomarkers, we aimed to better understand the molecular mechanisms underlying aneurysm formation.

Methods And Results: In Fibulin-4R/R mice, the extracellular matrix protein Fibulin-4 is 4-fold reduced, resulting in progressive ascending aneurysm formation and early death around 3 months of age. Read More

View Article

Anti-PCSK9 treatment: Is ultra-low LDL always good?

Cardiovasc Res 2018 Jun 20. Epub 2018 Jun 20.

Department of Bioscience Internal Medicine and Specialties, University of Palermo, Italy.

Anti-pcsk9 (proprotein convertase subtilisin kexin 9) monoclonal antibodies (Mab) are novel, potent lipid-lowering drugs. They demonstrated to improve the lipid profile in high cardiovascular risk patients. Anti-pcsk9 Mab inhibit the targeted LDL-receptor degradation induced by pcsk9 protein and are able to reduce LDL cholesterol (LDL-C) levels on top of conventional lipid-lowering therapy. Read More

View Article

Heart specific PGC-1α deletion identifies metabolome of cardiac restricted metabolic heart failure.

Cardiovasc Res 2018 Jun 20. Epub 2018 Jun 20.

A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.

Aims: Heart failure (HF) is associated with drastic changes in metabolism leading to a cardiac energy deficiency well as maladaptive changes in multiple other tissues. It is still unclear which of these changes originates from cardiomyocyte metabolic remodeling or whether they are induced secondarily by systemic factors. Our aim here was to induce cardiac restricted metabolic changes mimicking those seen in HF and to characterize the associated metabolite changes in the heart, circulation and peripheral tissues. Read More

View Article

Drebrin Regulates Angiotensin II-Induced Aortic Remodeling.

Cardiovasc Res 2018 Jun 20. Epub 2018 Jun 20.

Department of Medicine, Duke University Medical Center, Durham, NC USA 27710.

Aims: The actin-binding protein Drebrin is up-regulated in response to arterial injury and reduces smooth muscle cell (SMC) migration and proliferation through its interaction with the actin cytoskeleton. We therefore tested the hypothesis that SMC Drebrin inhibits angiotensin II-induced remodeling of the proximal aorta.

Methods And Results: Angiotensin II was administered via osmotic minipumps at 1000 ng/kg/min continuously for 28 days in SM22-Cre+/Dbnflox/flox (SMC-Dbn-/-) and control mice. Read More

View Article

A gene therapeutic approach to inhibit CIB1 ameliorates maladaptive remodeling in pressure overload.

Cardiovasc Res 2018 Jun 20. Epub 2018 Jun 20.

Klinik für Kardiologie und Angiologie, Germany.

Aims: Chronic heart failure is becoming increasingly prevalent and is still associated with a high mortality rate. Myocardial hypertrophy and fibrosis drive cardiac remodeling and heart failure, but they are not sufficiently inhibited by current treatment strategies. Furthermore, despite increasing knowledge on cardiomyocyte intracellular signaling proteins inducing pathological hypertrophy, therapeutic approaches to target these molecules are currently unavailable. Read More

View Article
June 2018
1 Read

VEGF Regulation of eNOS Phosphorylation Is Involved in Isoflurane Cardiac Preconditioning.

Cardiovasc Res 2018 Jun 21. Epub 2018 Jun 21.

Departments of Anesthesiology and Physiology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, Wisconsin, USA.

Aims: Previous studies indicate that nitric oxide derived from endothelial nitric oxide synthase (eNOS) serves as both trigger and mediator in anesthetic cardiac preconditioning. The mechanisms underlying regulation of eNOS by volatile anesthetics have not been fully understood. Therefore, this study examined the role of vascular endothelial growth factor (VEGF) in isoflurane cardiac preconditioning. Read More

View Article

Nrf2 deficiency impairs atherosclerotic lesion development but promotes features of plaque instability in hypercholesterolemic mice.

Cardiovasc Res 2018 Jun 18. Epub 2018 Jun 18.

A.I. Virtanen Institute, University of Eastern Finland, Kuopio, Finland.

Aims: Oxidative stress and inflammation play an important role in the progression of atherosclerosis. Transcription factor NF-E2-related factor 2 (Nrf2) has antioxidant and anti-inflammatory effects in the vessel wall, but paradoxically, global loss of Nrf2 in apoE deficient mice alleviates atherosclerosis. In this study, we investigated the effect of global Nrf2 deficiency on early and advanced atherogenesis in alternative models of atherosclerosis, LDL receptor deficient mice (LDLR-/-) and LDLR-/- mice expressing apoB-100 only (LDLR-/-ApoB100/100) having a humanized lipoprotein profile. Read More

View Article

Generation and primary characterization of iAM-1, a versatile new line of conditionally immortalized atrial myocytes with preserved cardiomyogenic differentiation capacity.

Cardiovasc Res 2018 Jun 18. Epub 2018 Jun 18.

Laboratory of Experimental Cardiology, Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, 2300 RC Leiden, the Netherlands.

Aims: The generation of homogeneous cardiomyocyte populations from fresh tissue or stem cells is laborious and costly. A potential solution to this problem would be to establish lines of immortalized cardiomyocytes. However, as proliferation and (terminal) differentiation of cardiomyocytes are mutually exclusive processes, their permanent immortalization causes loss of electrical and mechanical functions. Read More

View Article

Genome Wide Studies of Heart Failure and Endophenotypes: lessons learned and future directions.

Cardiovasc Res 2018 Apr 18. Epub 2018 Apr 18.

University of Groningen, University Medical Center Groningen, The department of Cardiology, Groningen, The Netherlands.

Heart failure (HF) is a complex clinical syndrome resulting from structural or functional impairments of ventricular filling or ejection of blood. HF has a poor prognosis and the burden to society remains tremendous. The unfulfilled expectation is that expanding our knowledge of the genetic architecture of HF will help to quickly advance the quality of risk assessment, diagnoses, and treatment. Read More

View Article

Metabolic changes in hypertrophic cardiomyopathies: Scientific update from the Working Group of Myocardial Function of the European Society of Cardiology.

Cardiovasc Res 2018 Jun 15. Epub 2018 Jun 15.

Netherlands Heart Institute, Utrecht, the Netherlands.

Disturbed metabolism as a consequence of obesity and diabetes may cause cardiac diseases (recently highlighted in the CVR spotlight issue on Metabolic cardiomyopathies).1 In turn, the metabolism of the heart may also be disturbed in genetic and acquired forms of hypertrophic cardiac disease. Here, we provide an overview of recent insights on metabolic changes in genetic hypertrophic cardiomyopathy (HCM) and discuss several therapies which may be explored to target disturbed metabolism and prevent onset of cardiac hypertrophy. Read More

View Article

Mechanical stretch on endothelial cells interconnects innate and adaptive immune response in hypertension.

Cardiovasc Res 2018 Jun 15. Epub 2018 Jun 15.

Center for Cardiology- Cardiology I, University Medical Center Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.

View Article

Reg-ulating macrophage infiltration to alter wound healing following myocardial infarction.

Authors:
Merry L Lindsey

Cardiovasc Res 2018 Jun 15. Epub 2018 Jun 15.

Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, 39216, USA.

View Article

Brain MRI fiber-tracking reveals white matter alterations in hypertensive patients without damage at conventional neuroimaging.

Cardiovasc Res 2018 Jun 12. Epub 2018 Jun 12.

Department of Angiocardioneurology and Translational Medicine, IRCCS Neuromed, Via dell'elettronica, 86077 Pozzilli (IS), Italy.

Aims: Hypertension is one of the main risk factor for dementia. The subtle damage provoked by chronic high blood pressure in the brain is usually evidenced by conventional magnetic resonance imaging (MRI), in terms of white matter (WM) hyperintensities or cerebral atrophy. However, it is clear that by the time brain damage is visible, it may be too late hampering neurodegeneration. Read More

View Article

Dr Giacomo Rossitto interviews Professor Rhian Touyz, on the translational applications of vascular smooth muscle cell biology in cardiovascular disease.

Cardiovasc Res 2018 May;114(6):e43

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

View Article
May 2018
2 Reads

High-sensitivity troponin: a barometer for cardiac health.

Cardiovasc Res 2018 May;114(6):e36-e38

BHF/University Centre for Cardiovascular Science, University of Edinburgh, Room SU.226, Chancellor's Building, Edinburgh EH16 4SB, UK.

View Article

The future of myocardial injury biomarkers in cardiovascular disease: looking beyond cardiac troponins.

Authors:
Michael Marber

Cardiovasc Res 2018 May;114(6):e39-e40

The Rayne Institute, St Thomas' Hospital, 4th Floor Lambeth Wing, Westminster Bridge Road, London SE1 7EH, UK.

View Article

Epigenetic control of lipid metabolism: implications for lifespan and healthspan.

Cardiovasc Res 2018 May;114(6):e33-e35

Department of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, 75390, Dallas, TX, USA.

View Article

Trained immunity and cardiovascular disease: is it time for translation to humans?

Cardiovasc Res 2018 May;114(6):e41-e42

Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, 20133 Milan, Italy.

View Article

Rapid Inhibition of Atherosclerotic Plaque Progression by Sonodynamic Therapy.

Cardiovasc Res 2018 Jun 6. Epub 2018 Jun 6.

Department of Cardiology, the First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, 150001, P. R. China.

Aims: Currently, efficient regimens to reverse atherosclerotic plaques are not available in the clinic. Here, we present sonodynamic therapy (SDT) as a novel methodology to rapidly inhibit progression of atherosclerotic plaques.

Methods And Results: In atherosclerotic rabbit and apoE-deficient mouse models, SDT efficiently decreased the atherosclerotic burden within one week, revealing a decrease in the size of the atherosclerotic plaque and enlarged lumen. Read More

View Article

Experimental models of murine atherosclerosis: does perception match reality?

Cardiovasc Res 2018 Jun 5. Epub 2018 Jun 5.

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Beech Hill Road, Sheffield, S10 2RX, United Kingdom.

Background: Murine models of atherosclerosis have been invaluable to gain mechanistic understanding of this chronic disease. Induction of atherosclerosis with relative ease in ApoE-/- and Ldlr-/- mice fed a Western-type diet to cause hyperlipidaemia has provided researchers with popular tools to manipulate and characterise the action of genes that affect atherogenesis. Seminal studies and reviews have discussed key phenotypic differences between different models and "target levels of hyperlipidaemia" have also been published. Read More

View Article

A novel method for high precision aortic constriction that allows for generation of specific cardiac phenotypes in mice.

Cardiovasc Res 2018 Jun 5. Epub 2018 Jun 5.

Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo.

Aims: Generation of reproducible cardiac disease phenotypes in mice is instrumental for investigating mechanisms leading to heart failure. For decades, suture-based thoracic aortic constriction has been the preferred method for increasing left ventricular (LV) afterload in rodents, but the degree of stenosis resulting from this method is variable. In an effort to improve this methodology, we subjected mice to constriction of the ascending aorta using o-rings with fixed inner diameters (IDs). Read More

View Article
June 2018
1 Read

Obesity-induced cardiac dysfunction: prenatal vs postnatal nurture.

Cardiovasc Res 2018 Jun 5. Epub 2018 Jun 5.

Department of Medicine, Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, MD, US.

View Article

Flow-related Right Ventricular - Pulmonary Arterial Pressure Gradients during Exercise.

Cardiovasc Res 2018 Jun 6. Epub 2018 Jun 6.

Institute of Medical Science, University of Toronto, Toronto, Canada.

Aims: The assumption of equivalence between right ventricular and pulmonary arterial systolic pressure is fundamental to several assessments of right ventricular or pulmonary vascular hemodynamic function. Our aims were to 1) determine whether systolic pressure gradients develop across the right ventricular outflow tract in healthy adults during exercise, 2) examine the potential correlates of such gradients, and 3) consider the effect of such gradients on calculated indices of right ventricular function.

Methods And Results: Healthy untrained and endurance-trained adult volunteers were studied using right-heart catheterization at rest and during submaximal cycle ergometry. Read More

View Article

Role of endothelial and macrophage tetrahydrobiopterin in development and progression of atherosclerosis - BH4 puzzle solved?

Cardiovasc Res 2018 Jun 5. Epub 2018 Jun 5.

University Medical Center Mainz, Center for Cardiology, Cardiology I, Mainz, Germany.

View Article
June 2018
2 Reads

Role of Genetics in the Prediction of Statin-Associated Muscle Symptoms and Optimization of Statin Use and Adherence.

Cardiovasc Res 2018 Jun 5. Epub 2018 Jun 5.

Mount Sinai Heart, Icahn School of Medicine at Mount Sinai, New York, NY USA.

Statin therapy reduces cardiovascular events in patients with, or at risk of, atherosclerotic cardiovascular disease. However, statins are underutilized in patients for whom they are indicated and are frequently discontinued. Discontinuation may be the result of the development of statin-associated muscle symptoms (SAMS), which encompass a broad spectrum of clinical phenotypes from myalgia to severe myopathy. Read More

View Article

Downregulation of BK Channel Function and Protein Expression in Coronary Arteriolar Smooth Muscle Cells of Type 2 Diabetic Patients.

Cardiovasc Res 2018 May 30. Epub 2018 May 30.

The Departments of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA.

Aims: Type 2 diabetes (T2D) is strongly associated with cardiovascular morbidity and mortality in patients. Vascular large conductance Ca2+-activated potassium (BK) channels, composed of four pore-forming α subunits (BK-α) and four regulatory β1 subunits (BK-β1), are densely expressed in coronary arterial smooth muscle cells (SMCs) and play an important role in regulating vascular tone and myocardial perfusion. However, the role of BK channels in coronary microvascular dysfunction of human subjects with diabetes is unclear. Read More

View Article

Nur77 protects against adverse cardiac remodelling by limiting Neuropeptide Y signalling in the sympathoadrenal-cardiac axis.

Cardiovasc Res 2018 May 30. Epub 2018 May 30.

Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Academic Medical Center, University of Amsterdam, The Netherlands.

Aims: Cardiac remodelling and heart failure are promoted by persistent sympathetic activity. We recently reported that nuclear receptor Nur77 may protect against sympathetic agonist-induced cardiac remodelling in mice. The sympathetic co-transmitter Neuropeptide Y (NPY) is co-released with catecholamines and is a known cardiac modulator and predictor of heart failure mortality. Read More

View Article

Reg proteins direct accumulation of functionally distinct macrophage subsets after myocardial infarction.

Cardiovasc Res 2018 May 30. Epub 2018 May 30.

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

Aims: Myocardial infarction (MI) causes a massive increase of macrophages in the heart, which serve various non-redundant functions for cardiac repair. The identities of signals controlling recruitment of functionally distinct cardiac macrophages to sites of injury are only partially known. Previous work identified Regenerating islet-derived protein 3 beta (Reg3β) as a novel factor directing macrophages to sites of myocardial injury. Read More

View Article

Teaching cardiovascular medicine to machines.

Authors:
Pablo Lamata

Cardiovasc Res 2018 May 30. Epub 2018 May 30.

United Kingdom.

View Article

Apoptotic cell induction of miR-10b in macrophages contributes to advanced atherosclerosis progression in ApoE-/- mice.

Cardiovasc Res 2018 May 30. Epub 2018 May 30.

Department of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou, PR China.

Aims: We previously found that miR-10b inhibits cholesterol efflux from thioglycollate-elicited mouse peritoneal macrophages through repressing ABCA1. Here, we deciphered the mechanism underlying macrophage miR-10b expression and the role of miR-10b in atherosclerosis.

Methods And Results: MiR-10b expression was increased in the arteries with advanced but not early atherosclerotic plaques of ApoE-/- mice. Read More

View Article

Reduction of Myocardial Ischemia-Reperfusion Injury by Inactivating Oxidized Phospholipids.

Cardiovasc Res 2018 May 30. Epub 2018 May 30.

Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, University of California San Diego, La Jolla, CA, USA.

Aims: Myocardial ischemia followed by reperfusion (IR) causes an oxidative burst resulting in cellular dysfunction. Little is known about the impact of oxidative stress on cardiomyocyte lipids and their role in cardiac cell death. Our goal was to identify oxidized phosphatidylcholine-containing phospholipids (OxPL) generated during IR, and to determine their impact on cell viability and myocardial infarct size. Read More

View Article
May 2018
1 Read

Complex Roads from Genotype to Phenotype in Dilated Cardiomyopathy: Scientific update from the Working Group of Myocardial Function of the European Society of Cardiology

Cardiovasc Res 2018 05 23. Epub 2018 May 23.

Department of Cardiology, Maastricht University Medical Center & CARIM, Maastricht University, Maastricht, The Netherlands.

Dilated cardiomyopathy (DCM) frequently affects relatively young, economically and socially active adults, and is an important cause of heart failure and transplantation. DCM is a complex disease and its pathological architecture encounters many genetic determinants interacting with environmental factors. The old perspective that every pathogenic gene mutation would lead to a diseased heart, is now being replaced by the novel observation that the phenotype depends not only on the penetrance -malignancy of the mutated gene- but also on epigenetics, age, toxic factors, pregnancy and a diversity of acquired diseases. Read More

View Article

Urocortin 2 - Will a Drug Targeting Both the Vasculature and the RV be the Future of PH Therapy?

Cardiovasc Res 2018 May 23. Epub 2018 May 23.

Program in Translational Lung Research, Department of Medicine, University of Colorado Anschutz Medical Campus.

View Article

Dr Anke Smits talks to Professor Johann Wojta on the benefits for young investigators at FCVB 2018.

Cardiovasc Res 2018 Jun;114(7):e56-55

Department of Internal Medicine II, Medical University of Vienna, Austria.

View Article

Recognizing young investigators at Frontiers in Cardiovascular Biology 2018.

Cardiovasc Res 2018 Jun;114(7):e53-e55

BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.

View Article

Catheter ablation of atrial fibrillation and outcomes in heart failure patients: seeking the treasure in the CASTLE.

Authors:
Stanley Nattel

Cardiovasc Res 2018 Jun;114(7):e50-e52

Department of Medicine and Research Center, Montreal Heart Institute and Université de Montréal, 5000 Bélanger Street East, Montreal, QC H1T 1C8, Canada.

View Article

Macrophages: new players in cardiac ageing?

Cardiovasc Res 2018 Jun;114(7):e47-e49

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.

View Article

Beyond longevity: novel roles of Sirtuin-3 in thrombosis.

Cardiovasc Res 2018 May 23. Epub 2018 May 23.

University Hospital Würzburg, Department of Internal Medicine, 97080 - Würzburg, Germany.

View Article

From lipid locus to drug target through human genomics.

Cardiovasc Res 2018 May 23. Epub 2018 May 23.

Department of Cardiology, University Medical Center Utrecht, University of Utrecht, Utrecht, the Netherlands.

In the last decade over 175 genetic loci have robustly been associated to levels of major circulating blood lipids. Most loci are specific to one or two lipids, while some (SUGP1, ZPR1, TRIB1, HERPUD1, and FADS1) are associated to all. While exposing the polygenic architecture of circulating lipids and the underpinnings of dyslipidemia, these genome-wide association studies (GWAS) have provided further evidence of the critical role that lipids play in coronary heart disease (CHD) risk, as indicated by the 2. Read More

View Article

Pregnancy and estrogen regulate sinoatrial node calcium homeostasis and accelerate pacemaking.

Cardiovasc Res 2018 May 23. Epub 2018 May 23.

Research Center, Montreal Heart Institute, 5000 Bélanger, Montréal, Québec, Canada, H1T 1C8.

Aims: During pregnancy, there is a significant increase in heart rate (HR) potentially associated with an increased risk of arrhythmias or exacerbation of pre-existing cardiac conditions endangering both mother and fetus. Calcium homeostasis plays an important role in regulating automaticity of the sinoatrial node (SAN) however, its contribution to the accelerated HR during pregnancy remains unknown.

Methods And Results: Using murine SAN cells, we showed that pregnancy increased L-type Ca2+ current (ICaL) and CaV1. Read More

View Article

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 05 23. Epub 2018 May 23.

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

Non-coding RNAs are increasingly recognized not only as regulators of various biological functions but also as targets for a new generation of RNA therapeutics and biomarkers. We hereby review recent insights relating to non-coding RNAs including microRNAs (e.g. Read More

View Article

Hypertension and increased endothelial mechanical stretch promote monocyte differentiation and activation: Roles of STAT3, interleukin 6 and hydrogen peroxide.

Cardiovasc Res 2018 May 23. Epub 2018 May 23.

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

Aims: Monocytes play an important role in hypertension. Circulating monocytes in humans exist as classical, intermediate and non-classical forms. Monocyte differentiation can be influenced by the endothelium, which in turn is activated in hypertension by mechanical stretch. Read More

View Article

Molecular Events that Lead to Cardiomyocyte Binucleation.

Cardiovasc Res 2018 May 23. Epub 2018 May 23.

Department of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, MA, USA.

View Article

PCSK9 expression in the ischemic heart and its relationship to infarct size, cardiac function and development of autophagy.

Cardiovasc Res 2018 May 24. Epub 2018 May 24.

Central Arkansas Veterans Healthcare System and the University of Arkansas for Medical Sciences, Little Rock, AR.

Background: Inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a novel therapy to treat hypercholesterolemia and related cardiovascular diseases. This study determined if PCSK9 can regulate infarct size, cardiac function and autophagy during ischemia.

Methods And Results: Mice hearts were subjected to left coronary artery (LCA) occlusion. Read More

View Article

Neutrophils recruited by leukotriene B4 induce features of plaque destabilization during endotoxemia.

Cardiovasc Res 2018 May 24. Epub 2018 May 24.

UMR 1148 INSERM, Xavier Bichat Hospital, 75018 Paris, France.

Aims: Both leukotrienes and neutrophils have been linked to plaque destabilization. Despite being evoked, the role of leukotriene B4 on neutrophil recruitment to plaques and the concomitant effects of these two actors on plaque stability remain to be proven. Since both actors are elicited during endotoxemia, a condition associated with the risk of cardiovascular events, we investigated whether endotoxemia promotes leukotriene B4-mediated neutrophil infiltration in plaques and explored the roles of leukotriene B4 and neutrophils in plaque destabilization. Read More

View Article

In the heart of the MEF2 transcription network: novel downstream effectors as potential targets for the treatment of cardiovascular disease.

Cardiovasc Res 2018 May 23. Epub 2018 May 23.

Institute of Genetic and Biomedical Research (IRGB), UOS Milan - National Research Council (CNR), Milan, Italy; Humanitas Research Hospital, Rozzano, Milan, Italy.

View Article

Functional role of endothelial CXCL16/CXCR6-platelet-leukocyte axis in angiotensin II-associated metabolic disorders.

Cardiovasc Res 2018 May 23. Epub 2018 May 23.

Department of Pharmacology, Faculty of Medicine, University of Valencia, Valencia, Spain.

Aim: Angiotensin-II (Ang-II) is the main effector peptide of the renin-angiotensin system (RAS) and promotes leukocyte adhesion to the stimulated endothelium. Because RAS activation and Ang-II signaling are implicated in metabolic syndrome (MS) and abdominal aortic aneurysm (AAA), we investigated the effect of Ang-II on CXCL16 arterial expression, the underlying mechanisms, and the functional role of the CXCL16/CXCR6 axis in these cardiometabolic disorders.

Methods And Results: Results from in vitro chamber assays revealed that CXCL16 neutralization significantly inhibited mononuclear leukocyte adhesion to arterial but not to venous endothelial cells. Read More

View Article

Sirtuin 1 Activation Attenuates Cardiac Fibrosis in a Rodent Pressure Overload Model by Modifying Smad2/3 Transactivation.

Cardiovasc Res 2018 May 25. Epub 2018 May 25.

Keenan Research Centre for Biomedical Science, St. Michael's Hospital, 209 Victoria Street, Toronto, ON, Canada M5B 1T8.

Aims: Transforming growth factor β1 (TGF-β1) is a prosclerotic cytokine involved in cardiac remodeling leading to heart failure (HF). Acetylation/de-acetylation of specific lysine residues in Smad2/3 has been shown to regulate TGF-β signaling by altering its transcriptional activity. Recently, the lysine de-acetylase sirtuin 1 (SIRT1) has been shown to have a cardioprotective effect; however SIRT1 expression and activity are paradoxically reduced in HF. Read More

View Article
May 2018
1 Read