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    10365 results match your criteria Cardiovascular research[Journal]

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    From genome-wide association studies to Mendelian randomization: Novel opportunities for understanding cardiovascular disease causality, pathogenesis, prevention, and treatment.
    Cardiovasc Res 2018 Feb 19. Epub 2018 Feb 19.
    The Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, Denmark.
    The Mendelian randomization approach is an epidemiologic study design incorporating genetic information into traditional epidemiologic studies to infer causality of biomarkers, risk factors, or lifestyle factors on disease risk. Mendelian randomization studies often draw on novel information generated in genome-wide association studies on causal associations between genetic variants and a risk factor or lifestyle factor. Such information can then be used in a largely unconfounded study design free of reverse causation to understand if and how risk factors and lifestyle factors cause cardiovascular disease. Read More

    Pathophysiological understanding of HFpEF: microRNAs as part of the puzzle.
    Cardiovasc Res 2018 Feb 16. Epub 2018 Feb 16.
    Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.
    Half of all heart failure patients have preserved ejection fraction (HFpEF). Comorbidities associated with and contributing to HFpEF include obesity, diabetes and hypertension. Still, the underlying pathophysiological mechanisms of HFpEF are unknown. Read More

    Non-genomic effects of nuclear receptors: insights from the anucleate platelet.
    Cardiovasc Res 2018 Feb 14. Epub 2018 Feb 14.
    Nuclear receptors have the ability to elicit two different kinds of responses, genomic and non-genomic. While genomic responses control gene expression by influencing the rate of transcription, non-genomic effects occur rapidly and independently of transcriptional regulation. Due to their anucleate nature and mechanistically well-characterised and rapid responses, platelets provide a model system for the study of any non-genomic effects of the nuclear receptors. Read More

    Vitamin D receptor restricts Th2-biased inflammation in the heart.
    Cardiovasc Res 2018 Feb 12. Epub 2018 Feb 12.
    The Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen 518060, China.
    Background And Aims: The aberrant immune responses play a critical role in the pathogenesis of myocarditis. Vitamin D receptor (VDR) has immune regulatory functions. This study aims to investigate the role of VDR in the restricting the immune inflammation in the heart. Read More

    Geranylgeranyl pyrophosphate synthase facilitates the organization of cardiomyocytes during mid-gestation through modulating protein geranylgeranylation in mouse heart.
    Cardiovasc Res 2018 Feb 12. Epub 2018 Feb 12.
    Ministry of Education Key Laboratory of Model Animals for Disease Study, Model Animal Research Center and Medical School of Nanjing University, National Resource Center for Mutant Mice, Nanjing, Jiangsu Province, 210093, People's Republic of China.
    Aims: With the maturation of placenta, ventricular chamber maturation enhances cardiac contractile performance to adapt to the metabolic demand of growing embryo. The organization of cardiomyocytes is required for the morphological remodeling in ventricular chamber maturation. However, the mechanism governing the establishment of cardiac cytoarchitecture during ventricular chamber maturation is still poorly studied. Read More

    Loss of Sirt3 accelerates arterial thrombosis by increasing formation of neutrophil extracellular traps and plasma tissue factor activity.
    Cardiovasc Res 2018 Feb 10. Epub 2018 Feb 10.
    Center for Molecular Cardiology, University of Zurich, Switzerland.
    Background: Sirtuin 3 (Sirt3) is a mitochondrial, nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that reduces oxidative stress by activation of superoxide dismutase 2 (SOD2). Oxidative stress enhances arterial thrombosis. This study investigated the effects of genetic Sirt3 deletion on arterial thrombosis in mice in an inflammatory setting and assessed the clinical relevance of these findings in patients with ST-elevation myocardial infarction (STEMI). Read More

    Cardioprotection by ischemic postconditioning and cGMP-elevating agents involves cardiomyocyte nitric oxide-sensitive guanylyl cyclase.
    Cardiovasc Res 2018 Feb 9. Epub 2018 Feb 9.
    Department of Pharmacology, Toxicology and Clinical Pharmacy, Institute of Pharmacy, University of Tübingen, Tübingen, Germany.
    Aims: It has been suggested that the nitric oxide-sensitive guanylyl cyclase (NO-GC)/cGMP-dependent signaling pathway affords protection against cardiac damage during acute myocardial infarction (AMI). It is, however, not clear whether the NO-GC/cGMP system confers its favorable effects through a mechanism located in cardiomyocytes (CMs). The aim of this study was to evaluate the infarct-limiting effects of the endogenous NO-GC in CMs in vivo. Read More

    Multiple common co-morbidities produce left ventricular diastolic dysfunction associated with coronary microvascular dysfunction, oxidative stress and myocardial stiffening.
    Cardiovasc Res 2018 Feb 8. Epub 2018 Feb 8.
    Division of Experimental Cardiology, Department of Cardiology.
    Rationale: More than 50% of patients with heart failure have preserved ejection fraction characterized by diastolic dysfunction. The prevalance of diastolic dysfunction is higher in females and associates with multiple comorbidities such as hypertension (HT), obesity, hypercholesterolemia (HC) and diabetes mellitus (DM), although its pathophysiology remains incompletely understood. It has been proposed that the co-morbidities induce systemic inflammation, cardiac microvascular dysfunction and oxidative stress, leading to myocardial fibrosis, myocyte stiffening and ultimately, diastolic dysfunction. Read More

    Biomechanical defects and rescue of cardiomyocytes expressing pathologic nuclear lamins.
    Cardiovasc Res 2018 Feb 8. Epub 2018 Feb 8.
    Department of Engineering and Architecture; University of Trieste; Trieste (Italy).
    Aims: Given the clinical impact of LMNA cardiomyopathies, understanding lamin function will fulfill a clinical need and will lead to advancement in the treatment of heart failure. A multidisciplinary approach combining cell biology, atomic force microscopy (AFM) and molecular modeling was used to analyze the biomechanical properties of human lamin A/C gene (LMNA) mutations (E161K, D192G, N195K) using an in vitro neonatal rat ventricular myocyte (NRVM) model.

    Methods And Results: The severity of biomechanical defects due to the three LMNA mutations correlated with the severity of the clinical phenotype. Read More

    Osteoglycin Attenuates Cardiac Fibrosis by Suppressing Cardiac myofibroblast proliferation and migration throughAntagonizing LPA3/MMP2/EGFR signaling.
    Cardiovasc Res 2018 Feb 5. Epub 2018 Feb 5.
    Department of Hypertension, Ruijin Hospital and Shanghai Institute of Hypertension, Shanghai JiaoTong University School of Medicine, Shanghai 200025, China.
    Aims: Cardiac myofibroblasts (CMFs) play a crucial role in the progression of pathological fibrotic cardiac remodeling. The expression of osteoglycin (OGN) is increased in diseased hearts; however, the role of OGN in pathological cardiac remodeling is not understood. Here we sought to determine the effect of OGN on cardiac interstitial fibrosis and investigated the molecular mechanisms of OGN in CMF activation and matrix production. Read More

    Critical role of Phosphodiesterase 2A in mouse congenital heart defects.
    Cardiovasc Res 2018 Feb 2. Epub 2018 Feb 2.
    Department of Anatomical, Histological, Forensic and Orthopaedic Sciences, Sapienza University of Rome, 00161 Rome, Italy.
    Aims: Phosphodiesterase 2A, a cAMP-hydrolysing enzyme, is essential for mouse development, however the cause of Pde2A knockout embryonic lethality is unknown. To understand if Pde2A plays a role in cardiac development, hearts of Pde2A deficient embryos were analysed at different stage of development.

    Methods And Results: At the stage of four chambers, Pde2A deficient hearts were enlarged compared to the hearts of Pde2A heterozygous and wild-type. Read More

    Cardiomyocyte Specific Deletion of Sirt1 Gene Sensitizes Myocardium to Ischemia and Reperfusion Injury.
    Cardiovasc Res 2018 Feb 2. Epub 2018 Feb 2.
    Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216.
    Aim: A longevity gene, Sirtuin 1 (SIRT1) and energy sensor AMP-activated protein kinase (AMPK) have common activators such as caloric restriction, oxidative stress and exercise. The objective of this study is to characterize the role of cardiomyocyte SIRT1 in age-related impaired ischemic AMPK activation and increased susceptibility to ischemic insults.

    Methods And Results: Mice were subjected to ligation of left anterior descending coronary artery for in vivo ischemic models. Read More

    Stretch-induced compliance: a novel adaptive biological mechanism following acute cardiac load.
    Cardiovasc Res 2018 Feb 1. Epub 2018 Feb 1.
    Department of Surgery and Physiology & Cardiovascular Research Centre, Faculty of Medicine, University of Porto, Portugal.
    Aims: The heart is constantly challenged with acute bouts of stretching or overload. Systolic adaptations to these challenges are known but adaptations in diastolic stiffness remain unknown. We evaluated adaptations in myocardial stiffness due to acute stretching and characterized the underlying mechanisms. Read More

    Vascular Smooth Muscle Contraction in Hypertension.
    Cardiovasc Res 2018 Jan 31. Epub 2018 Jan 31.
    Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
    Hypertension is a major risk factor for many common chronic diseases, such as heart failure, myocardial infarction, stroke, vascular dementia and chronic kidney disease. Pathophysiological mechanisms contributing to the development of hypertension include increased vascular resistance, determined in large part by reduced vascular diameter due to increased vascular contraction and arterial remodelling. These processes are regulated by complex interacting systems such as the renin angiotensin aldosterone system (RAAS), sympathetic nervous system, immune activation and oxidative stress, which influence vascular smooth muscle function. Read More

    Smooth Muscle Cell Fate and Plasticity in Atherosclerosis.
    Cardiovasc Res 2018 Jan 27. Epub 2018 Jan 27.
    Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
    Current knowledge suggests that intimal smooth muscle cells (SMCs) in native atherosclerotic plaque derive mainly from the medial arterial layer. During this process, SMCs undergo complex structural and functional changes giving rise to a broad spectrum of phenotypes. Classically, intimal SMCs are described as dedifferentiated/synthetic SMCs, a phenotype characterized by reduced expression of contractile proteins. Read More

    New models to study vascular mural cell embryonic origin: implications in vascular diseases.
    Cardiovasc Res 2018 Jan 27. Epub 2018 Jan 27.
    Laboratory of Angiogenesis and Redox Metabolism, Department of Biology, University of Padua, Via U. Bassi 58/b, 35131, Padova, Italy.
    A key question in vascular biology is how the diversity of origin of vascular mural cells, namely smooth muscle cells and pericytes influences vessel properties, in particular the regional propensity to vascular diseases. This review therefore first describes the role and regulation of mural cells during vascular formation, with a focus on embryonic origin. We then consider the evidence that connects heterogeneities in smooth muscle cell and pericyte origins with disease. Read More

    Dynamic and Diverse Changes in the Functional Properties of Vascular Smooth Muscle Cells in Pulmonary Hypertension.
    Cardiovasc Res 2018 Jan 27. Epub 2018 Jan 27.
    Pulmonary and Critical Care Medicine, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
    Pulmonary hypertension (PH) is the end result of interaction between pulmonary vascular tone and a complex series of cellular and molecular events termed "vascular remodeling". The remodeling process, which can involve the entirety of pulmonary arterial vasculature, almost universally involves medial thickening, driven by increased numbers and hypertrophy of its principal cellular constituent, smooth muscle cells (SMCs). It is noted, however that SMCs comprise heterogeneous populations of cells, which can exhibit markedly different proliferative, inflammatory, and extracellular matrix production changes during remodeling. Read More

    Integrated transcriptomic and regulatory network analyses identify microRNA-200c as a novel repressor of human pluripotent stem cell-derived cardiomyocyte differentiation and maturation.
    Cardiovasc Res 2018 Jan 24. Epub 2018 Jan 24.
    School of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
    Aims: MicroRNAs (miRNAs) are crucial for the post-transcriptional control of protein-encoding genes, and together with transcription factors (TFs) regulate gene expression; however, the regulatory activities of miRNAs during cardiac development are only partially understood. In this study, we tested the hypothesis that integrative computational approaches could identify miRNAs that experimentally could be shown to regulate cardiomyogenesis.

    Methods And Results: We integrated expression profiles with bioinformatics analyses of miRNA and TF regulatory programs to identify candidate miRNAs involved with cardiac development. Read More

    Role of smooth muscle cells in coronary artery bypass grafting failure.
    Cardiovasc Res 2018 Jan 24. Epub 2018 Jan 24.
    Bristol Medical School, Research Floor Level 7, Bristol Royal Infirmary, Bristol, BS2 8HW.
    Atherosclerosis is the underlying pathology of many cardiovascular diseases. The formation and rupture of atherosclerotic plaques in the coronary arteries results in angina and myocardial infarction. Venous coronary artery bypass grafts (CABG) are designed to reduce the consequences of atherosclerosis in the coronary arteries by diverting blood flow around the atherosclerotic plaques. Read More

    Stat5-dependent Cardioprotection in Late Remote Ischemia Preconditioning.
    Cardiovasc Res 2018 Jan 22. Epub 2018 Jan 22.
    Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing 210023, China;.
    Aims: To study the protective effects of late remote ischemic preconditioning (RIPC) against myocardial ischemia/reperfusion (I/R) injury and determine whether Stat5 is involved in this protection by using cardiomyocyte-specific Stat5 knockout mice (Stat5-cKO).

    Methods And Results: Mice were exposed to lower limb RIPC or sham ischemia. After 24 hours, the left anterior descending artery (LAD) was ligated for 30 minutes, then reperfused for 180 minutes. Read More

    Identification of cardiac long non-coding RNA profile in human dilated cardiomyopathy.
    Cardiovasc Res 2018 Jan 22. Epub 2018 Jan 22.
    Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
    Aims: Dilated cardiomyopathy (DCM) induced chronic heart failure is a life-threatening disease worldwide. Long non-coding RNAs (lncRNAs) are potential new therapeutic targets and may provide new pathophysiological mechanisms for development of DCM.

    Methods And Results: Microarray assays in 14 DCM and 10 control human heart samples identified 313 significantly differentially expressed lncRNAs. Read More

    Endogenous Sonic Hedgehog limits inflammation and angiogenesis in the ischemic skeletal muscle of mice.
    Cardiovasc Res 2018 Jan 22. Epub 2018 Jan 22.
    Univ. Bordeaux, Inserm, Biology of Cardiovascular Diseases, U1034, CHU de Bordeaux, F-33604 Pessac, France.
    Aim: The purpose of the present study was to investigate the role of endogenous Shh in ischemia-induced angiogenesis.

    Methods And Results: To this aim, we used inducible Shh knock-out (KO) mice and unexpectedly found that capillary density was significantly increased in regenerating muscle of Shh deficient mice 5 days after hind limb ischemia (HLI) was induced, demonstrating that endogenous Shh does not promote angiogenesis but more likely limits it. Myosin and MyoD expression were equivalent in Shh deficient mice and control mice, indicating that endogenous Shh is not required for ischemia-induced myogenesis. Read More

    Targeted endothelial gene deletion of Triggering Receptor Expressed on Myeloid cells-1 protects mice during septic shock.
    Cardiovasc Res 2018 Jan 19. Epub 2018 Jan 19.
    INSERM UMRS-1116, Faculté de Médecine Nancy, Université de Lorraine, Nancy, France.
    Aims: TREM-1 (Triggering Receptor Expressed on Myeloid cells-1) is an immunoreceptor expressed on neutrophils and monocytes/macrophages whose role is to amplify the inflammatory response driven by Toll-Like Receptors engagement. The pharmacological inhibition of TREM-1 confers protection in several pre-clinical models of acute inflammation. In this study, we aimed to decipher the role of TREM-1 on the endothelium. Read More

    Elevated plasma catecholamines functionally compensate for the reduced myogenic tone in smooth muscle STIM1 knockout mice but with deleterious cardiac effects.
    Cardiovasc Res 2018 Jan 19. Epub 2018 Jan 19.
    Department of Physiology, University of Tennessee Health Sciences Center, Memphis, TN 38163.
    Aims: Stromal interaction molecule 1 (STIM1) has emerged as an important player in the regulation of growth and proliferation of smooth muscle cells. Therefore, we hypothesized that STIM1 plays a crucial role in the maintenance of vascular integrity. The objective of this study was to evaluate whether reduced expression of STIM1 could modify the structure and function of the vasculature, leading to changes in blood pressure (BP). Read More

    Vascular smooth muscle cell death, autophagy and senescence in atherosclerosis.
    Cardiovasc Res 2018 Jan 18. Epub 2018 Jan 18.
    Laboratory of Physiopharmacology, University of Antwerp, Universiteitsplein 1, B-2610 Antwerp, Belgium.
    In the present review, we describe the causes and consequences of loss of vascular smooth muscle cells (VSMCs) or their function in advanced atherosclerotic plaques, and discuss possible mechanisms such as cell death or senescence, and induction of autophagy to promote cell survival. We also highlight the potential use of pharmacological modulators of these processes to limit plaque progression and/or improve plaque stability. VSMCs play a pivotal role in atherogenesis. Read More

    Transcriptional Regulation of Stress Kinase JNK2 in Pro-Arrhythmic CaMKIIδ Expression in the Aged Atrium.
    Cardiovasc Res 2018 Jan 19. Epub 2018 Jan 19.
    Department of Physiology & Biophysics, Rush University Medical Center, Chicago, IL.
    Introduction: c-jun N-terminal kinase (JNK) is a critical stress response kinase that activates in a wide range of physiological and pathological cellular processes. We recently discovered a pivotal role of JNK in the development of atrial arrhythmias in the aged heart, while cardiac CaMKIIδ, another pro-arrhythmic molecule, was also found to enhance atrial arrhythmogenicity. Here, we aimed to reveal a regulatory role of the stress kinase JNK2 isoform on CaMKIIδ expression. Read More

    Loss of KCNK3 is a hallmark of RV hypertrophy/dysfunction associated with pulmonary hypertension.
    Cardiovasc Res 2018 Jan 19. Epub 2018 Jan 19.
    Univ. Paris-Sud, Faculté de Médecine, Kremlin-Bicêtre, France.
    Aims: Mutations in the KCNK3 gene, which encodes for an outward-rectifier K+ channel, have been identified in patients suffering from pulmonary arterial hypertension (PAH), and constitute the first described channelopathy in PAH. In human PAH and experimental pulmonary hypertension (PH), we demonstrated that KCNK3 expression and function are severely reduced in pulmonary vascular cells, promoting PH-like phenotype at the morphologic and hemodynamic levels. Since KCNK3 channel is also expressed in both the human and rodent heart, we aimed to elucidate the pathophysiological role of KCNK3 channel in right ventricular (RV) hypertrophy (RVH) related to PH. Read More

    Electrical Coupling between Cardiomyocytes and Fibroblasts: Experimental Testing of a Challenging and Important Concept.
    Cardiovasc Res 2018 Jan 17. Epub 2018 Jan 17.
    Department of Medicine and Research Center, Montreal Heart Institute and Université de Montréal, Montreal, Canada; Department of Pharmacology and Therapeutics, McGill University Montreal, Canada; Institute of Pharmacology, West German Heart and Vascular Center, Faculty of Medicine, University Duisburg-Essen, Essen, Germany.

    IL-6 trans-activation contributes to aldosterone induced cardiac fibrosis.
    Cardiovasc Res 2018 Jan 19. Epub 2018 Jan 19.
    Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
    Aims: An excess of aldosterone results in cardiac remodeling and fibrosis. Interleukin-6 (IL-6) is a key mediator in the fibrotic process, however the effect of aldosterone on the expression of IL-6 remains unclear. We investigated whether aldosterone induces the expression of IL-6 and thereby contributes to the fibrotic process. Read More

    From genetics to response to injury: vascular smooth muscle cells in aneurysms and dissections of the ascending aorta.
    Cardiovasc Res 2018 Jan 17. Epub 2018 Jan 17.
    Division of Medical Genetics Department of Internal Medicine University of Texas Medical School at Houston, Houston, Texas, USA 77030, e-mail:
    Vascular Smooth Muscle Cells (vSMCs) play a crucial role in both the pathogenesis of Aneurysms and Dissections of the ascending thoracic aorta (TAAD) in humans and in the associated adaptive compensatory responses, since thrombosis and inflammatory processes are absent in the majority of cases. Aneurysms and dissections share numerous characteristics, including aetiologies and histopathological alterations: vSMC disappearance, medial areas of mucoid degeneration, and ExtraCellular Matrix (ECM) breakdown. Three aetiologies predominate in TAAD in humans: i) genetic causes in heritable familial forms, ii) an association with bicuspid aortic valves and iii) a sporadic degenerative form linked to the aortic aging process. Read More

    Smooth muscle cells of intracranial vessels: From development to disease.
    Cardiovasc Res 2018 Jan 16. Epub 2018 Jan 16.
    Genetics and Pathogenesis of Cerebrovascular Diseases, INSERM, Université Paris Diderot-Paris 7, Paris, France and DHU NeuroVasc, Sorbonne Paris Cité, Paris, France.
    Cerebrovascular diseases that cause ischemic or hemorrhagic stroke with subsequent loss of life or functional capacity due to damage of the brain tissue are among the leading causes of human suffering and economic burden inflicted by diseases in the developed world. Diseases affecting intracranial vessels are significant contributors to ischemic and hemorrhagic strokes. Brain arteriovenous malformations (bAVM), which are a collection of abnormal blood vessels connecting arteries to veins, are the most common cause of intracranial hemorrhage in children and young adults. Read More

    DOCA-salt hypertension activates PlGF in the spleen to couple sympathetic drive and immune system activation.
    Cardiovasc Res 2018 Jan 8. Epub 2018 Jan 8.
    Department of Angiocardioneurology and Translational Medicine, IRCCS Neuromed, 86077 Pozzilli (IS), Italy.
    Aims: Chronic increase of mineralocorticoids obtained by administration of Deoxycorticosterone acetate (DOCA) results in salt dependent hypertension in animals. Despite the lack of a generalized sympathoexcitation, DOCA-salt hypertension has been also associated to overdrive of peripheral nervous system in organs typically targeted by blood pressure (BP), as kidneys and vasculature. Aim of this study was to explore whether DOCA-salt recruits immune system by overactivating sympathetic nervous system in lymphoid organs and whether this is relevant for hypertension. Read More

    Exploring immune checkpoints as potential therapeutic targets in atherosclerosis.
    Cardiovasc Res 2017 Dec 22. Epub 2017 Dec 22.
    Department of Medical Biochemistry, Experimental Vascular Biology, Academic Medical Center, University of Amsterdam, the Netherlands.
    In the past decades, the inflammatory nature of atherosclerosis has been well recognized and despite the development of therapeutic strategies targeted at its classical risk factors such as dyslipidemia and hypertension, atherosclerosis remains a major cause of morbidity and mortality. Additional strategies targeting the chronic inflammatory pathways underlying the development of atherosclerosis are therefore required. Interactions between different immune cells result in the secretion of inflammatory mediators, such as cytokines and chemokines, and fuel atherogenesis. Read More

    Endothelial-Mesenchymal Transition in Atherosclerosis.
    Cardiovasc Res 2018 Jan 4. Epub 2018 Jan 4.
    Laboratory for Cardiovascular Regenerative Medicine, Dept. Pathology and Medical biology, University Medical Center Groningen, University of Groningen, The Netherlands.
    Atherosclerosis is an inflammatory disease resulting in the hardening and thickening of the wall of arteries and the formation of plaques, which comprise of immune cells, mesenchymal cells, lipids and extracellular matrix (ECM). The source of mesenchymal cells in the atherosclerotic plaques have been under scrutiny for years. Current endothelial-lineage tracing studies indicate that the endothelium is a source for plaque-associated mesenchymal cells. Read More

    Non-coding RNAs: key regulators of smooth muscle cell fate in vascular disease.
    Cardiovasc Res 2017 Dec 29. Epub 2017 Dec 29.
    Technical University Munich, Department of Vascular and Endovascular Surgery, Klinikum rechts der Isar, Munich, Germany.
    The vascular smooth muscle cell (SMC) is one of the most plastic cells in the body. Understanding how non-coding RNAs regulate SMC cell-fate decision making in the vasculature has significantly enhanced our understanding of disease development, and opened up exciting new avenues for potential therapeutic applications. Recent studies on SMC physiology have in addition challenged our traditional view on their role and contribution to vascular disease, mainly in the setting of atherosclerosis as well as aneurysm disease, and restenosis after angioplasties. Read More

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