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    10298 results match your criteria Cardiovascular research[Journal]

    1 OF 206

    Meox1 accelerates myocardial hypertrophic decompensation through Gata4.
    Cardiovasc Res 2017 Nov 16. Epub 2017 Nov 16.
    Key Laboratory of Human Disease Comparative Medicine, NHFPC, Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences & Comparative Medical Center, Peking Union Medical College, China.
    Aims: Pathological hypertrophy is the result of gene network regulation, which ultimately leads to adverse cardiac remodelling and heart failure (HF), and is accompanied by the reactivation of a 'foetal gene programme'. The Mesenchyme homeobox 1 (Meox1) gene is one of the foetal programme genes. Meox1 may play a role in embryonic development, but its regulation of pathological hypertrophy is not known. Read More

    Local production of tenascin-C acts as a trigger for monocyte/macrophage recruitment that provokes cardiac dysfunction.
    Cardiovasc Res 2017 Nov 10. Epub 2017 Nov 10.
    I2MC, Toulouse University, Inserm, UPS, Toulouse, France.
    Aims: Tenascin-C (TNC) is an endogenous danger signal molecule strongly associated with inflammatory diseases and with poor outcome in patients with cardiomyopathies. Its function within pathological cardiac tissue during pressure overload remains poorly understood.

    Methods And Results: We showed that TNC accumulates after 1 week of transverse aortic constriction (TAC) in the heart of 12-week-old male mice. Read More

    Atheroprone flow activates inflammation via endothelial ATP-dependent P2X7-p38 signalling.
    Cardiovasc Res 2017 Nov 6. Epub 2017 Nov 6.
    Department of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Beech Hill Road, Sheffield, S10 2RX, UK.
    Objective: Atherosclerosis is a focal disease occurring at arterial sites of disturbed blood flow that generates low oscillating shear stress. Endothelial inflammatory signalling is enhanced at sites of disturbed flow via mechanisms that are incompletely understood. The influence of disturbed flow on endothelial ATP receptors and downstream signalling was assessed. Read More

    Central and Peripheral Slow-Pressor Mechanisms Contributing to.
    Cardiovasc Res 2017 Nov 8. Epub 2017 Nov 8.
    Brain and Heart Research Group, University of Ottawa Heart Institute, Ottawa, ON, Canada.
    Aims: High salt intake markedly enhances hypertension induced by angiotensin II (Ang II). We explored central and peripheral slow-pressor mechanisms which may be activated by Ang II and salt.

    Methods And Results: In Protocol I, Wistar rats were infused subcutaneously with low- dose Ang II (150 ng/kg/min) and fed regular (0. Read More

    Extracellular vesicles in diagnostics and therapy of the ischaemic heart: Position Paper from the Working Group on Cellular Biology of the Heart of the European Society of Cardiology.
    Cardiovasc Res 2017 Nov 2. Epub 2017 Nov 2.
    Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary; and Pharmahungary Group, Szeged, Hungary.
    Extracellular vesicles (EVs) - particularly exosomes and microvesicles - are attracting considerable interest in the cardiovascular field as the wide range of their functions is recognized. These capabilities include transporting regulatory molecules including different RNA species, lipids, and proteins through the extracellular space including blood and delivering these cargos to recipient cells to modify cellular activity. EVs powerfully stimulate angiogenesis, and can protect the heart against myocardial infarction. Read More

    Transplantation of brown adipose tissue inhibits atherosclerosis in apoE-/- mice: contribution of the activated FGF-21-adiponectin axis.
    Cardiovasc Res 2017 Nov 2. Epub 2017 Nov 2.
    Department of Cardiovascular Medicine, Graduate School of Medical Science.
    Aims: Brown adipose tissue (BAT) has been identified as an endocrine organ that maintains metabolic homeostasis; however, the effects on atherosclerosis remain undefined. Here, we investigated the effect of experimental BAT transplantation on atherosclerosis.

    Methods And Results: Interscapular BAT was dissected from 12-week-old wild-type mice and transplanted into the visceral cavity of 12-week-old apoE-/- mice. Read More

    Sonic hedgehog-dependent activation of adventitial fibroblasts promotes neointima formation.
    Cardiovasc Res 2017 Nov;113(13):1653-1663
    Vascular Remodeling and Regeneration Group, Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany.
    Aims: Adventitial cells have been suggested to contribute to neointima formation, but the functional relevance and the responsible signalling pathways are largely unknown. Sonic hedgehog (Shh) is a regulator of vasculogenesis and promotes angiogenesis in the adult.

    Methods And Results: Here we show that proliferation of vascular smooth muscle cells (SMC) after wire-induced injury in C57BL/6 mice is preceded by proliferation of adventitial fibroblasts. Read More

    Insights into innate immune signalling in controlling cardiac remodelling.
    Cardiovasc Res 2017 Nov;113(13):1538-1550
    Department of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuchang District, Wuhan 430060, People's Republic of China.
    Canonical innate immune signalling involves complex cascades: multiple germline-encoded pattern recognition receptors rapidly recognize pathogen-associated or damage-associated molecular patterns to induce the production of cytokines, which bind to their corresponding receptors to orchestrate subsequent host defense phases. Inflammation is a healthy response to pathogenic signals, which are typically rapid and specific, and they terminate once the threat has passed. However, excessive activation or suppression of innate immune or inflammatory responses can lead to considerable human suffering, such as cardiac remodelling. Read More

    Interleukin-9 mediates chronic kidney disease-dependent vein graft disease: a role for mast cells.
    Cardiovasc Res 2017 Nov;113(13):1551-1559
    Cardiology, Department of Medicine.
    Aims: Chronic kidney disease (CKD) is a powerful independent risk factor for cardiovascular events, including vein graft failure. Because CKD impairs the clearance of small proteins, we tested the hypothesis that CKD exacerbates vein graft disease by elevating serum levels of critical cytokines that promote vein graft neointimal hyperplasia.

    Methods And Results: We modelled CKD in C57BL/6 mice with 5/6ths nephrectomy, which reduced glomerular filtration rate by 60%, and we modelled vein grafting with inferior-vena-cava-to-carotid interposition grafting. Read More

    Obesity-induced vascular dysfunction and arterial stiffening requires endothelial cell arginase 1.
    Cardiovasc Res 2017 Nov;113(13):1664-1676
    Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.
    Aims: Elevation of arginase activity has been linked to vascular dysfunction in diabetes and hypertension by a mechanism involving decreased nitric oxide (NO) bioavailability due to L-arginine depletion. Excessive arginase activity also can drive L-arginine metabolism towards the production of ornithine, polyamines, and proline, promoting proliferation of vascular smooth muscle cells and collagen formation, leading to perivascular fibrosis. We hypothesized that there is a specific involvement of arginase 1 expression within the vascular endothelial cells in this pathology. Read More

    Loss of Protein Kinase Novel 1 (PKN1) is Associated with Mild Systolic and Diastolic Contractile Dysfunction, Increased Phospholamban Thr17 Phosphorylation and Exacerbated Ischaemia-Reperfusion Injury.
    Cardiovasc Res 2017 Oct 16. Epub 2017 Oct 16.
    School of Cardiovascular Medicine and Sciences, British Heart Foundation Centre for Research Excellence, Department of Cardiology, Faculty of Life Sciences and Medicine, King's College London, The Rayne Institute, St Thomas's Hospital, Lambeth Palace Road, London SE1 7EH, UK.
    Aims: PKN1 is a stress-responsive protein kinase acting downstream of small GTP-binding proteins of the Rho/Rac family. The aim was to determine its role in endogenous cardioprotection.

    Methods And Results: Hearts from PKN1 knockout (KO) or wild type (WT) littermate control mice were perfused in Langendorff mode and subjected to global ischemia and reperfusion (I/R). Read More

    Both cardiomyocyte and endothelial cell Nox4 mediate protection against hemodynamic overload-induced remodeling.
    Cardiovasc Res 2017 Oct 13. Epub 2017 Oct 13.
    King's College London British Heart Foundation Centre of Excellence, London, UK.
    Aims: NADPH oxidase-4 (Nox4) is an important reactive oxygen species (ROS) source that is upregulated in the hemodynamically overloaded heart. Our previous studies using global Nox4 knockout (Nox4KO) mice demonstrated a protective role of Nox4 during chronic abdominal aortic banding, involving a paracrine enhancement of myocardial capillary density. However, other authors who studied cardiac-specific Nox4KO mice reported detrimental effects of Nox4 in response to transverse aortic constriction (TAC). Read More

    Title: Therapeutic strategies utilising SDF-1α in ischaemic cardiomyopathy.
    Cardiovasc Res 2017 Oct 13. Epub 2017 Oct 13.
    The Hatter Cardiovascular Institute, 67 Chenies Mews, University College London, London, United Kingdom, WC1E 6HX.
    Heart failure is rapidly increasing in prevalence and will redraw the global landscape for cardiovascular health. Alleviating and repairing cardiac injury associated with myocardial infarction (MI) is key to improving this burden. Homing signals mobilise and recruit stem cells to the ischaemic myocardium where they exert beneficial paracrine effects. Read More

    Luma is not essential for murine cardiac development and function.
    Cardiovasc Res 2017 Oct 12. Epub 2017 Oct 12.
    University of California San Diego. School of Medicine. 9500 Gilman Drive. CA 92093 La Jolla. USA.
    Aims: Luma is a recently discovered, evolutionarily conserved protein expressed in mammalian heart that is associated with the LInker of Nucleoskeleton and Cytoskeleton (LINC) complex. The LINC complex structurally integrates the nucleus and the cytoplasm, and plays a critical role in mechanotransduction across the nuclear envelope. Mutations in several LINC components in both humans and mice result in various cardiomyopathies, implying they play essential, non-redundant roles. Read More

    CD40L controls obesity-associated vascular inflammation, oxidative stress and endothelial dysfunction in mice - translational aspects for man.
    Cardiovasc Res 2017 Sep 26. Epub 2017 Sep 26.
    Center for Cardiology, Molecular Cardiology.
    Aims: CD40 ligand (CD40L) signaling controls vascular oxidative stress and related dysfunction in angiotensin-II-induced arterial hypertension by regulating vascular immune cell recruitment and platelet activation. Here we investigated the role of CD40L in experimental hyperlipidemia.

    Methods And Results: Male wild type and CD40L-/- mice (C57BL/6 background) were subjected to high fat diet for sixteen weeks. Read More

    Identification of optimal reference genes for transcriptomic analyses in normal and diseased human heart.
    Cardiovasc Res 2017 Sep 22. Epub 2017 Sep 22.
    Inserm, UMR-S 1180, Univ. Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.
    Aims: Quantitative real-time RT-PCR (RT-qPCR) has become the method of choice for mRNA quantification, but requires an accurate normalization based on the use of reference genes showing invariant expression across various pathological conditions. Only few data exist on appropriate reference genes for the human heart. The objective of this study was to determine a set of suitable reference genes in human atrial and ventricular tissues, from right and left cavities in control and in cardiac diseases. Read More

    Deficit in PINK1-PARKIN mediated mitochondrial autophagy at late stages of dystrophic cardiomyopathy.
    Cardiovasc Res 2017 Oct 5. Epub 2017 Oct 5.
    Department of Pharmacology, Physiology and Neuroscience, New Jersey Medical School - Rutgers University, Newark, NJ, USA.
    Aims: Duchenne Muscular Dystrophy (DMD) is an inherited devastating muscle disease with severe and often lethal cardiac complications. Emerging evidence suggests that the evolution of the pathology in DMD is accompanied by the accumulation of mitochondria with defective structure and function. Here we investigate whether defects in the housekeeping autophagic pathway contribute to mitochondrial and metabolic dysfunctions in dystrophic cardiomyopathy. Read More

    IL-1R and MyD88 signaling in CD4+ T cells promote Th17 immunity and atherosclerosis.
    Cardiovasc Res 2017 Sep 28. Epub 2017 Sep 28.
    Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Jan Waldenströms gata 35, 20502 Malmö, Sweden.
    Aims: The role of CD4+ T cells in atherosclerosis has been shown to be dependent on cytokine cues that regulate lineage commitment into mature T helper subsets. In this study we tested the roles of IL-1R1 and MyD88 signaling in CD4+ T cells in atherosclerosis.

    Methods And Results: We transferred apoe-/-myd88+/+or apoe-/-myd88-/- CD4+ T cells to T- and B-cell-deficient rag1-/-apoe-/- mice fed high fat diet. Read More

    Cgnl1, an endothelial junction complex protein, regulates GTPase mediated angiogenesis.
    Cardiovasc Res 2017 Aug 31. Epub 2017 Aug 31.
    Department of Cardiology, Thoraxcenter, University Medical Center Utrecht, The Netherlands.
    Aims: The formation of cell-cell and cell-extra cellular matrix contacts by endothelial cells is crucial for the stability and integrity of a vascular network. We previously identified cingulin-like 1 (Cgnl1) in a transcriptomic screen for new angiogenic modulators. Here we aim to study the function of the cell-cell junction associated protein Cgnl1 during vessel formation. Read More

    The HAND1 frameshift A126FS mutation does not cause hypoplastic left heart syndrome in mice.
    Cardiovasc Res 2017 Aug 31. Epub 2017 Aug 31.
    Departments of Pediatrics, Anatomy, Biochemistry, and Medical and Molecular Genetics, Riley Heart Research Center, Herman B Wells Center for Pediatric Research, Indiana School of Medicine, 1044 W. Walnut St., Indianapolis, IN 46202-5225, USA.
    Aims: To test if a human Hand1 frame shift mutation identified in human samples is causative of hypoplastic left heart syndrome (HLHS).

    Methods And Results: HLHS is a poorly understood single ventricle congenital heart defect that affects two to three infants in every 10 000 live births. The aetiologies of HLHS are largely unknown. Read More

    miR-30c-5p regulates macrophage-mediated inflammation and pro-atherosclerosis pathways.
    Cardiovasc Res 2017 Nov;113(13):1627-1638
    Department of Medicine, DIMED, University of Padova, via Giustiniani, 2, 35128 Padova, Italy.
    Aims: Atherosclerosis is an inflammatory disease wherein cholesterol-loaded macrophages play a major role. MicroRNAs and microparticles propagate inflammatory pathways and are involved in cardiovascular disease. We aimed to screen and validate circulating microRNAs correlated with atherosclerosis development in humans, and to dissect the molecular mechanisms associated with atherogenesis using in vitro and in vivo approaches. Read More

    Cardiac troponins: from myocardial infarction to chronic disease.
    Cardiovasc Res 2017 Sep 14. Epub 2017 Sep 14.
    BHF Centre of Research Excellence, Cardiovascular Division, King's College London, London, UK.
    Elucidation of the physiologically distinct subunits of troponin in 1973 greatly facilitated our understanding of cardiac contraction. Although troponins are expressed in both skeletal and cardiac muscle, there are isoforms of troponin I/T expressed selectively in the heart. By exploiting cardiac-restricted epitopes within these proteins, one of the most successful diagnostic tests to-date has been developed: cardiac troponin (cTn) assays. Read More

    Cardiac effects of SGLT2 inhibitors: the sodium hypothesis.
    Cardiovasc Res 2017 Aug 4. Epub 2017 Aug 4.
    Clinic for Internal Medicine III, University of the Saarland, Homburg 66421, Germany.
    The effects of intense glycaemic control on macrovascular complications in patients with type 2 diabetes are incompletely resolved, and many glucose-lowering medications negatively affect cardiovascular outcomes. Recently, the EMPA-REG OUTCOME trial revealed that empagliflozin, an inhibitor of the sodium-glucose cotransporter 2 (SGLT2), substantially reduced the risk of hospitalization for heart failure, death from cardiovascular causes, and all-cause mortality in patients with type 2 diabetes mellitus at high cardiovascular risk. Although several mechanisms may explain this benefit, plasma volume contraction and a metabolic switch favouring cardiac ketone bodies oxidation have recently been proposed as the major drivers. Read More

    Differential Enos-Signalling by Platelet Subpopulations Regulates Adhesion and Aggregation.
    Cardiovasc Res 2017 Sep 4. Epub 2017 Sep 4.
    Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, T6G-2E1, CAN.
    Aims: In addition to maintaining hemostasis, circulating blood platelets are the cellular culprits that form occlusive thrombi in arteries and veins. Compared to blood leukocytes, which exist as functionally distinct subtypes, platelets are considered to be relatively simple cell fragments that form vascular system plugs without a differentially regulated cellular response. Hence, investigation into platelet subpopulations with distinct functional roles in hemostasis/thrombosis has been limited. Read More

    CXCL12-CXCR4 signalling plays an essential role in proper patterning of aortic arch and pulmonary arteries.
    Cardiovasc Res 2017 Nov;113(13):1677-1687
    Lee Gil Ya Cancer and Diabetes Institute, Gachon University, 155 Gaetbeol-ro, Yeonsu-gu, Incheon 21999, Republic of Korea.
    Aims: Chemokine CXCL12 (stromal derived factor 1: SDF1) has been shown to play important roles in various processes of cardiovascular development. In recent avian studies, CXCL12 signalling has been implicated in guidance of cardiac neural crest cells for their participation in the development of outflow tract and cardiac septum. The goal of this study is to investigate the extent to which CXCL12 signalling contribute to the development of aortic arch and pulmonary arteries in mammals. Read More

    Novel effects of dapagliflozin on epicardial adipose tissue with insulin resistance, high levels of inflammatory chemokines production and low differentiation ability.
    Cardiovasc Res 2017 Sep 11. Epub 2017 Sep 11.
    Cardiology Group, Health Research Institute of Santiago de Compostela.
    Aims: In patients with cardiovascular disease, epicardial adipose tissue (EAT) is characterized by insulin resistance, high pro-inflammatory chemokines and low differentiation ability. Since dapagliflozin reduces body fat and cardiovascular events in diabetic patients, we wanted to know its effect on EAT and subcutaneous adipose tissue (SAT).

    Methods And Results: Adipose samples were obtained from 52 patients undergoing heart surgery. Read More

    Semaphorin-3E Attenuates Neointimal Formation via Suppressing VSMCs Migration and Proliferation.
    Cardiovasc Res 2017 Sep 15. Epub 2017 Sep 15.
    Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
    Aims: The migration and proliferation of vascular smooth muscle cells (VSMCs) are crucial events in the neointimal formation, a hallmark of atherosclerosis and restenosis. Semaphorin3E (Sema3E) has been found to be a critical regulator of cell migration and proliferation in many scenarios. However, its role on VSMCs migration and proliferation is unclear. Read More

    A novel fibroblast growth factor-1 ligand with reduced heparin binding protects the heart against ischemia-reperfusion injury in the presence of heparin co-administration.
    Cardiovasc Res 2017 Nov;113(13):1585-1602
    Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
    Aims: Fibroblast growth factor 1 (FGF1), a heparin/heparan sulfate-binding growth factor, is a potent cardioprotective agent against myocardial infarction (MI). The impact of heparin, the standard of care for MI patients entering the emergency room, on cardioprotective effects of FGF1 is unknown, however.

    Methods And Results: To address this, a rat model of MI was employed to compare cardioprotective potentials (lower infarct size and improve post-ischemic function) of native FGF1 and an engineered FGF1 (FGF1ΔHBS) with reduced heparin-binding affinity when given at the onset of reperfusion in the absence or presence of heparin. Read More

    Diverging effects of enalapril or eplerenone in primary prevention against doxorubicin-induced cardiotoxicity.
    Cardiovasc Res 2017 Sep 7. Epub 2017 Sep 7.
    Service of Cardiology, Cardiovascular Department, Lausanne University Hospital (CHUV) Lausanne, Switzerland.
    Aims: Clinical studies suggest beneficial effects of renin-angiotensin system blockade for prevention of left ventricular (LV) dysfunction after chemotherapy. However, the efficacy of this strategy as primary prevention has been poorly studied. This study aimed at identifying the pathophysiological mechanisms by which mineralocorticoid receptor antagonism (MRA) or angiotensin converting enzyme inhibition (ACEi) provide protection against doxorubicin-induced cardiotoxicity (DIC) in mouse models of acute and chronic toxicity. Read More

    LncRNA TUG1 sponges miR-204-5p to promote osteoblast differentiation through upregulating Runx2 in aortic valve calcification.
    Cardiovasc Res 2017 Sep 4. Epub 2017 Sep 4.
    Department of Cardiovascular Surgery, Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China.
    Aims: Emerging evidence indicates that long non-coding RNAs (lncRNAs) play a vital role in cardiovascular physiology and pathology. Although the lncRNA TUG1 is implicated in atherosclerosis, its function in calcific aortic valve disease (CAVD) remains unknown.

    Methods And Results: In this study, we found that TUG1 was highly expressed in human aortic valves and primary valve interstitial cells (VICs). Read More

    Endothelial to haematopoietic transition contributes to pulmonary arterial hypertension.
    Cardiovasc Res 2017 Nov;113(13):1560-1573
    Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine.
    Aims: The pathogenic mechanisms of pulmonary arterial hypertension (PAH) remain unclear, but involve dysfunctional endothelial cells (ECs), dysregulated immunity and inflammation in the lung. We hypothesize that a developmental process called endothelial to haematopoietic transition (EHT) contributes to the pathogenesis of pulmonary hypertension (PH). We sought to determine the role of EHT in mouse models of PH, to characterize specific cell types involved in this process, and to identify potential therapeutic targets to prevent disease progression. Read More

    Regulation of vascular smooth muscle cell calcification by syndecan-4/FGF-2/PKCα signalling and cross-talk with TGFβ.
    Cardiovasc Res 2017 Nov;113(13):1639-1652
    Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
    Aims: Vascular calcification is a major cause of morbidity and mortality. Fibroblast growth factor-2 (FGF-2) plays an instructive role in osteogenesis and bone development, but its role in vascular calcification was unknown. Therefore, we investigated the involvement of FGF-2 in vascular calcification and determined the mechanism by which it regulates this process. Read More

    Electrical coupling between ventricular myocytes and myofibroblasts in the infarcted mouse heart.
    Cardiovasc Res 2017 Sep 1. Epub 2017 Sep 1.
    Wells Centre for Pediatric Research, Indiana University School of Medicine, 1044 West Walnut Street, Indianapolis, IN 46202, USA.
    Aims: Recent studies have demonstrated electrotonic coupling between scar tissue and the surrounding myocardium in cryoinjured hearts. However, the electrical dynamics occurring at the myocyte-nonmyocyte interface in the fibrotic heart remain undefined. Here, we sought to develop an assay to interrogate the nonmyocyte cell type contributing to heterocellular coupling and to characterize, on a cellular scale, its voltage response in the infarct border zone of living hearts. Read More

    MicroRNA-424(322) as a new marker of disease progression in pulmonary arterial hypertension and its role in right ventricular hypertrophy by targeting SMURF1.
    Cardiovasc Res 2017 Sep 12. Epub 2017 Sep 12.
    CNC.IBILI, University of Coimbra, Portugal.
    Aims: MicroRNAs (miRNAs) have been implicated in the pathogenesis of pulmonary hypertension (PH), a multifactorial and progressive condition associated with an increased afterload of the right ventricle leading to heart failure and death. The main aim of this study was to correlate the levels of miR-424(322) with the severity and prognosis of PH and with right ventricle hypertrophy progression. Additionally, we intended to evaluate the mechanisms and signaling pathways whereby miR-424(322) secreted by pulmonary endothelial cells (PAECs) impacts cardiomyocytes. Read More

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