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    10226 results match your criteria Cardiovascular research[Journal]

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    Female ClockΔ19/Δ19 Mice are Protected from the Development of Age-Dependent Cardiomyopathy.
    Cardiovasc Res 2017 Sep 12. Epub 2017 Sep 12.
    Centre for Cardiovascular Investigations, Department of Biomedical Sciences, University of Guelph, Canada.
    Aims: Circadian rhythms are important for healthy cardiovascular physiology and they are regulated by the molecular circadian mechanism. Previously, we showed that disruption of the circadian mechanism factor CLOCK in male Clock Δ19/Δ19 mice led to development of age-dependent cardiomyopathy. Here, we investigate the role of biological sex in protecting against heart disease in aging female Clock Δ19/Δ19 mice. Read More

    A role for autoantibodies in atherogenesis.
    Cardiovasc Res 2017 Aug;113(10):1102-1112
    Faculty of Medicine and Public Health, The University of Newcastle, Callaghan, NSW 2308, Australia.
    An increased risk of cardiovascular disease (CVD) has long been recognized amongst people with autoimmune disease. It has been unclear whether this is due mainly to the ensuing treatment, particularly steroids, or whether some of this risk is due to the autoimmune process itself with subsequent inflammation. Indeed, a large body of evidence supports a role for chronic inflammation in atherogenesis, and autoantibodies have been identified as mediators in this complex inflammatory environment. Read More

    RHOA-ROCK signalling is necessary for lateralization and differentiation of the developing sinoatrial node.
    Cardiovasc Res 2017 Aug;113(10):1186-1197
    Department of Anatomy & Embryology, Leiden University Medical Center, Leiden, The Netherlands.
    Aims: RHOA-ROCK signalling regulates cell migration, proliferation, differentiation, and transcription. RHOA is expressed in the developing cardiac conduction system in chicken and mice. In early development, the entire sinus venosus myocardium, including both the transient left-sided and the definitive sinoatrial node (SAN), has pacemaker potential. Read More

    Angiotensin II infusion into ApoE-/- mice: a model for aortic dissection rather than abdominal aortic aneurysm?
    Cardiovasc Res 2017 Aug;113(10):1230-1242
    IBiTech-bioMMeda, Ghent University-iMinds Medical IT, De Pintelaan 185 Blok B, 9000 Ghent, Belgium.
    Aims: Angiotensin II-infused ApoE-/- mice are a popular mouse model for preclinical aneurysm research. Here, we provide insight in the often-reported but seldom-explained variability in shape of dissecting aneurysms in these mice.

    Methods And Results: N = 45 excised aortas were scanned ex vivo with phase-contrast X-ray tomographic microscopy. Read More

    The expression of the rare caveolin-3 variant T78M alters cardiac ion channels function and membrane excitability.
    Cardiovasc Res 2017 Aug;113(10):1256-1265
    Department of Biosciences, The PaceLab, Università degli Studi di Milano, Milano, Italy.
    Aims: Caveolinopathies are a family of genetic disorders arising from alterations of the caveolin-3 (cav-3) gene. The T78M cav-3 variant has been associated with both skeletal and cardiac muscle pathologies but its functional contribution, especially to cardiac diseases, is still controversial. Here, we evaluated the effect of the T78M cav-3 variant on cardiac ion channel function and membrane excitability. Read More

    Uncovering the arrhythmogenic potential of TRPM4 activation in atrial-derived HL-1 cells using novel recording and numerical approaches.
    Cardiovasc Res 2017 Aug;113(10):1243-1255
    Department of Physiology, Fukuoka University School of Medicine, 7-45-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan.
    Aims: Transient receptor potential cation channel subfamily melastatin member 4 (TRPM4), a Ca2+-activated nonselective cation channel abundantly expressed in the heart, has been implicated in conduction block and other arrhythmic propensities associated with cardiac remodelling and injury. The present study aimed to quantitatively evaluate the arrhythmogenic potential of TRPM4.

    Methods And Results: Patch clamp and biochemical analyses were performed using expression system and an immortalized atrial cardiomyocyte cell line (HL-1), and numerical model simulation was employed. Read More

    Serotonin and catecholamines in the development and progression of heart valve diseases.
    Cardiovasc Res 2017 Jul;113(8):849-857
    Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
    Heart valve diseases (HVDs) arise from a number of different processes that affect both the structure and function of the valve apparatus. Despite diverse aetiologies, treatments for HVDs are limited to percutaneous or surgical interventions. The search for medical therapies to prevent or slow the progression of HVDs has been hampered by our poor understanding of the progression from subclinical to symptomatic phases, and our limited knowledge of the molecular signals that control the susceptibility of valve interstitial cells to pathological remodeling. Read More

    Etv2 as an essential regulator of mesodermal lineage development.
    Cardiovasc Res 2017 Sep;113(11):1294-1306
    Lillehei Heart Institute, Department of Medicine, University of Minnesota, 2231 6th st. SE, Minneapolis, MN 55455, USA.
    The 'master regulatory factors' that position at the top of the genetic hierarchy of lineage determination have been a focus of intense interest, and have been investigated in various systems. Etv2/Etsrp71/ER71 is such a factor that is both necessary and sufficient for the development of haematopoietic and endothelial lineages. As such, genetic ablation of Etv2 leads to complete loss of blood and vessels, and overexpression can convert non-endothelial cells to the endothelial lineage. Read More

    Amyloidogenic medin induces endothelial dysfunction and vascular inflammation through the receptor for advanced glycation endproducts.
    Cardiovasc Res 2017 Sep;113(11):1389-1402
    Institute of Integrative Biology, University of Liverpool, Liverpool, UK.
    Aims: Medin is a common amyloidogenic protein in humans that accumulates in arteries with advanced age and has been implicated in vascular degeneration. Medin's effect on endothelial function remains unknown. The aims are to assess medin's effects on human arteriole endothelial function and identify potential mechanisms underlying medin-induced vascular injury. Read More

    Human induced pluripotent stem cell-derived vascular smooth muscle cells: differentiation and therapeutic potential.
    Cardiovasc Res 2017 Sep;113(11):1282-1293
    Department of Cardiovascular and Renal Research, University of Southern Denmark, J.B. Winslowvej 21 3, DK-5000 Odense, Denmark.
    Cardiovascular diseases remain the leading cause of death worldwide and current treatment strategies have limited effect of disease progression. It would be desirable to have better models to study developmental and pathological processes and model vascular diseases in laboratory settings. To this end, human induced pluripotent stem cells (hiPSCs) have generated great enthusiasm, and have been a driving force for development of novel strategies in drug discovery and regenerative cell-therapy for the last decade. Read More

    Melatonin as a cardioprotective therapy following ST-segment elevation myocardial infarction: is it really promising? Reply.
    Cardiovasc Res 2017 Sep;113(11):1418-1419
    The Hatter Cardiovascular Institute, University College London, London, UK; The National Institute of Health Research University College London Hospitals Biomedical Research Centre, London, UK; Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore, Singapore; and National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore; Department of Cardiology, Vall d'Hebron University Hospital and Research Institute. Universitat Autònoma, Barcelona, Spain; Department of Cardiology, Aarhus University Hospital Skejby, DK-8200, Aarhus N, Denmark; The Hatter Cardiovascular Institute, University College London, London, UK; Department of Physiology and Cell Biology, College of Medicine, University of South Alabama, Mobile, AL, USA; Experimental Renal and Cardiovascular Research, Department of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany; Duke University, Durham, NC, USA; Department of Medicine, Hatter Institute for Cardiovascular Research in Africa and South African Medical Research Council Inter-University Cape Heart Group, Faculty of Health Sciences, University of Cape Town, Chris Barnard Building, Anzio Road, Observatory, 7925, Cape Town, Western Cape, South Africa; Tamman Cardiovascular Research Institute, Sheba Medical Center, Tel Hashomer, Israel; Neufeld Cardiac Research Institute, Tel-Aviv University, Sheba Medical Center, Tel Hashomer, Israel; Sheba Center for Regenerative Medicine, Stem Cell, and Tissue Engineering, Tel Hashomer, Israel; Institute of Cardiology and Center of Excellence on Aging, 'G. d'Annunzio' University - Chieti, Italy; Texas Heart Institute and University of Texas Medical School in Houston, Department of Internal Medicine, Houston, TX, USA; Explorations Fonctionnelles Cardiovasculaires, Hôpital Louis Pradel, Lyon, France UMR 1060 (CarMeN), Université Claude Bernard, Lyon, France; Division of Cardiology, Department of Advanced Biomedical Sciences, Federico II University, Naples, Italy; University of Angers, University Hospital of Angers, Department of Cardiology, Angers, France; Institute of Physiology, Justus-Liebig University of Giessen, Giessen, Germany; Cardiology and UMC Utrecht Regenerative Medicine Center, University Medical Center Utrecht, the Netherlands; University Medical Center Utrecht, Division Heart and Lungs, and Hubrecht Institute, Utrecht, the Netherlands; Division of Cardiothoracic Surgery, Department of Surgery, Emory University, Atlanta, GA, USA; The Hatter Cardiovascular Institute, University College London, London, UK; and The National Institute of Health Research University College London Hospitals Biomedical Research Centre, London, UK; Cardiovascular Research Group, Department of Medical Biology, UiT, The Arctic University of Norway, Tromsø, Norway; Institute for Pathophysiology, West-German Heart and Vascular Center, University Hospital Essen, Essen, Germany; Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary; and Pharmahungary Group, Szeged, Hungary.

    CCAAT/enhancer-binding protein delta promotes intracellular lipid accumulation in M1 macrophages of vascular lesions.
    Cardiovasc Res 2017 Sep;113(11):1376-1388
    Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
    Aims: Lipid homeostasis is reprogrammed in the presence of inflammation, which results in excessive lipid accumulation in macrophages, and leads to the formation of lipid-laden foam cells. We aimed to link an inflammation-responsive transcription factor CCAAT/enhancer-binding protein delta (CEBPD) with polarized macrophages and dissect its contribution to lipid accumulation.

    Methods And Results: We found that CEBPD protein colocalized with macrophages in human and mouse (C57BL/6, Apoe-/-) atherosclerotic plaques and that Cebpd deficiency in bone marrow cells suppressed atherosclerotic lesions in hyperlipidemic Apoe-/- mice. Read More

    Impaired calcium homeostasis is associated with sudden cardiac death and arrhythmias in a genetic equivalent mouse model of the human HRC-Ser96Ala variant.
    Cardiovasc Res 2017 Sep;113(11):1403-1417
    Department of Molecular Biology, Center of Basic Research, Biomedical Research Foundation, Academy of Athens, Soranou Efessiou 4, 115 27, Athens, Greece.
    Aims: The histidine-rich calcium-binding protein (HRC) Ser96Ala variant has previously been identified as a potential biomarker for ventricular arrhythmias and sudden cardiac death in patients with idiopathic dilated cardiomyopathy. Herein, the role of this variant in cardiac pathophysiology is delineated through a novel mouse model, carrying the human mutation in the homologous mouse position.

    Methods And Results: The mouse HRC serine 81, homologous to human HRC serine 96, was mutated to alanine, using knock-in gene targeting. Read More

    Exosomes secreted by cardiomyocytes subjected to ischaemia promote cardiac angiogenesis.
    Cardiovasc Res 2017 Sep;113(11):1338-1350
    Institute for Biomedical Imaging and Life Sciences (IBILI), University of Coimbra, Azinhaga de Sta Comba, 3000-354 Coimbra, Portugal.
    Aims: Myocardial infarction (MI) is the leading cause of morbidity and mortality worldwide and results from an obstruction in the blood supply to a region of the heart. In an attempt to replenish oxygen and nutrients to the deprived area, affected cells release signals to promote the development of new vessels and confer protection against MI. However, the mechanisms underlying the growth of new vessels in an ischaemic scenario remain poorly understood. Read More

    The role of infiltrating immune cells in dysfunctional adipose tissue.
    Cardiovasc Res 2017 Jul;113(9):1009-1023
    British Heart Foundation Centre for Excellence, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, Scotland, UK.
    Adipose tissue (AT) dysfunction, characterized by loss of its homeostatic functions, is a hallmark of non-communicable diseases. It is characterized by chronic low-grade inflammation and is observed in obesity, metabolic disorders such as insulin resistance and diabetes. While classically it has been identified by increased cytokine or chemokine expression, such as increased MCP-1, RANTES, IL-6, interferon (IFN) gamma or TNFα, mechanistically, immune cell infiltration is a prominent feature of the dysfunctional AT. Read More

    The role of mineralocorticoid receptor signaling in the cross-talk between adipose tissue and the vascular wall.
    Cardiovasc Res 2017 Jul;113(9):1055-1063
    Diabetes and Cardiovascular Center, University of Missouri School of Medicine, Columbia, MO 65212, USA.
    Vascular dysfunction and impaired endothelial mediated relaxation are powerful underlying abnormalities in the pathogenesis of hypertension, coronary heart disease, and stroke. Obesity, type 2 diabetes mellitus, and other metabolic abnormalities are associated with activation of mineralocorticoid receptor (MRs) in the vasculature and adipose tissue. While MR signaling is involved in the normal physiological differentiation and maturation of adipocyte, enhanced activation of MRs also contributes to increase oxidative stress, release of pro-inflammatory adipokines, and dysregulation of adipocyte autophagy. Read More

    The interplay between adipose tissue and the cardiovascular system: is fat always bad?
    Cardiovasc Res 2017 Jul;113(9):999-1008
    Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK.
    Obesity is a risk factor for cardiovascular disease (CVD). However, clinical research has revealed a paradoxically protective role for obesity in patients with chronic diseases including CVD, suggesting that the biological 'quality' of adipose tissue (AT) may be more important than overall AT mass or body weight. Importantly, AT is recognised as a dynamic organ secreting a wide range of biologically active adipokines, microRNAs, gaseous messengers, and other metabolites that affect the cardiovascular system in both endocrine and paracrine ways. Read More

    Gingival fibroblasts protect against experimental abdominal aortic aneurysm development and rupture through tissue inhibitor of metalloproteinase-1 production.
    Cardiovasc Res 2017 Sep;113(11):1364-1375
    Inserm U970, Paris Cardiovascular Research Center, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
    Aims: Abdominal aortic aneurysm (AAA), frequently diagnosed in old patients, is characterized by chronic inflammation, vascular cell apoptosis and metalloproteinase-mediated extracellular matrix destruction. Despite improvement in the understanding of the pathophysiology of aortic aneurysm, no pharmacological treatment is yet available to limit dilatation and/or rupture. We previously reported that human gingival fibroblasts (GFs) can reduce carotid artery dilatation in a rabbit model of elastase-induced aneurysm. Read More

    Enhanced endothelin-1/Rho-kinase signalling and coronary microvascular dysfunction in hypertensive myocardial hypertrophy.
    Cardiovasc Res 2017 Sep;113(11):1329-1337
    Department of Medical Physiology, Texas A&M University Health Science Center, Temple, TX, USA.
    Aims: Hypertensive cardiac hypertrophy is associated with reduced coronary flow reserve, but its impact on coronary flow regulation and vasomotor function remains incompletely understood and requires further investigation.

    Methods And Results: Left ventricular hypertrophy was induced in mice by transverse aortic coarctation (TAC) for 4 weeks. The left coronary artery blood velocity (LCABV) and myocardium lactate level were measured following the metabolic activation by isoproterenol. Read More

    Diabetic db/db mice do not develop heart failure upon pressure overload: a longitudinal in vivo PET, MRI, and MRS study on cardiac metabolic, structural, and functional adaptations.
    Cardiovasc Res 2017 Aug;113(10):1148-1160
    Department of Biomedical Engineering, Biomedical NMR, Eindhoven University of Technology, PO Box 513, 5600 MB Eindhoven, The Netherlands.
    Aims: Heart failure is associated with altered myocardial substrate metabolism and impaired cardiac energetics. Comorbidities like diabetes may influence the metabolic adaptations during heart failure development. We quantified to what extent changes in substrate preference, lipid accumulation, and energy status predict the longitudinal development of hypertrophy and failure in the non-diabetic and the diabetic heart. Read More

    The molecular mechanisms of obesity paradox.
    Cardiovasc Res 2017 Jul;113(9):1074-1086
    1st Cardiology Department, Hippokration Hospital, Athens Medical School, Athens, Greece.
    Clinical observations suggest a complex relationship between human obesity and cardiovascular disease. Whilst abdominal (visceral) adiposity leads to deleterious metabolic disturbances, subcutaneous fat accumulation has a benign effect on cardiometabolic risk. Notably, an accumulating body of evidence paradoxically links increased body mass index with a better prognosis in patients with established cardiovascular disease, a finding that has been termed the 'obesity paradox'. Read More

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