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    16736 results match your criteria Circulation research[Journal]

    1 OF 335

    Stable Oxidative Cytosine Modifications Accumulate in Cardiac Mesenchymal Cells from Type2 Diabetes Patients: Rescue by Alpha-Ketoglutarate and TET-TDG Functional Reactivation.
    Circ Res 2017 Nov 20. Epub 2017 Nov 20.
    Division of Cardiovascular Epigenetics, Goethe University
    Rationale: Human cardiac mesenchymal cells (CMSCs) are a therapeutically-relevant primary cell population. Diabetes compromises CMSC function as consequence of metabolic alterations and incorporation of stable epigenetic changes. Objective: To investigate the role of α-ketoglutarate (αKG) in the epi-metabolic control of DNA demethylation in CMSCs. Read More

    Quaking Inhibits Doxorubicin-Mediated Cardiotoxicity Through Regulation of Cardiac Circular RNA Expression.
    Circ Res 2017 Nov 13. Epub 2017 Nov 13.
    Institute of Molecular and Translational Therapeutic Strategies, Hannover Medical School
    Rationale: RNA-binding proteins (RBPs) have been described to be expressed and regulated in various organs including the heart. Little is known about the role of RBPs in heart failure induced by the chemotherapy drug doxorubicin and their interaction with circular RNAs. Objective: We aimed to identify key RBPs involved in doxorubicin-mediated heart failure and to elucidate their function. Read More


    Induced Pluripotent Stem Cell (iPSC)-Derived Extracellular Vesicles Are Safer and More Effective for Cardiac Repair than iPSCs.
    Circ Res 2017 Nov 8. Epub 2017 Nov 8.
    Biochemistry, Biophysics and Biotechnology, Jagiellonian University.
    Rationale: Extracellular vesicles (EVs) are tiny membrane-enclosed droplets released by cells through membrane budding or exocytosis. The myocardial reparative abilities of EVs derived from induced pluripotent stem cells (iPSCs) have not been directly compared with the source iPSCs. Objective: To examine whether iPSC-derived EVs can influence the biological functions of cardiac cells in vitro; and compare the safety and efficacy of iPSC-EVs and iPSCs for cardiac repair in vivo. Read More

    Mitochondrial Oxidative Stress Reduces the Immunopotency of Mesenchymal Stromal Cells in Adults with Coronary Artery Disease.
    Circ Res 2017 Nov 7. Epub 2017 Nov 7.
    Medicine, McGill University
    Rationale: Mesenchymal stromal cells (MSCs) are promising therapeutic strategies for coronary artery disease (CAD), however, donor-related variability in cell quality is a main cause of discrepancies in preclinical studies. In vitro, MSCs from individuals with CAD have reduced ability to suppress activated T-cells. The mechanisms underlying the altered immunomodulatory capacity of MSCs in the context of atherosclerosis (ATH) remain elusive. Read More

    Associations of Endogenous Estradiol and Testosterone Levels with Plaque Composition and Risk of Stroke in Subjects with Carotid Atherosclerosis.
    Circ Res 2017 Nov 2. Epub 2017 Nov 2.
    Epidemiology, Erasmus MC.
    Rationale: Sex steroids may play a role in plaque composition and in stroke incidence. Objective: To study the associations of endogenous estradiol and testosterone with carotid plaque composition in elderly men and postmenopausal women with carotid atherosclerosis, as well as with risk of stroke in this population. Methods and Results: Data of 1023 postmenopausal women and 1124 men (≥45 years) with carotid atherosclerosis, from prospective population-based Rotterdam Study, were available. Read More

    Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induces Post-Translational Modifications of AKAP121, DRP1 and OPA1 That Promote Mitochondrial Fission.
    Circ Res 2017 Nov 1. Epub 2017 Nov 1.
    Fraternal Order of Eagles Diabetes Research Center, University of Iowa Carver College of Medicine
    Rationale: Cardiac lipotoxicity, characterized by increased uptake, oxidation and accumulation of lipid intermediates, contributes to cardiac dysfunction in obesity and diabetes. However, mechanisms linking lipid overload and mitochondrial dysfunction are incompletely understood. Objective: To elucidate the mechanisms for mitochondrial adaptations to lipid overload in postnatal hearts in vivo. Read More

    Unspliced XBP1 Confers VSMC Homeostasis and Prevents Aortic Aneurysm Formation via FoxO4 Interaction.
    Circ Res 2017 Oct 31. Epub 2017 Oct 31.
    Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University
    Rationale: Although not fully understood, the phenotypic transition of vascular smooth muscle cells exhibits at the early onset of the pathology of aortic aneurysms. Exploring the key regulators that are responsible for maintaining the contractile phenotype of VSMCs may confer vascular homeostasis and prevent aneurysmal disease. X-box binding protein 1, which exists in a transcriptionally inactive unspliced form (XBP1u) and a spliced active form (XBP1s), is a key component in response to endoplasmic reticular (ER) stress. Read More

    Thyroid Function and the Risk of Atherosclerotic Cardiovascular Morbidity and Mortality: The Rotterdam Study.
    Circ Res 2017 Oct 31. Epub 2017 Oct 31.
    Epidemiology, Erasmus Medical Center.
    Rationale: Thyroid hormones have been linked with various proatherogenic and antiatherogenic processes. However, the relationship of thyroid function with manifestations of atherosclerosis remains unclear. Objective: To investigate the association of thyroid function with atherosclerosis throughout its spectrum; i. Read More

    PVDOMICS: A Multi-Center Study to Improve Understanding of Pulmonary Vascular Disease Through Phenomics.
    Circ Res 2017 Oct;121(10):1136-1139
    From the Vanderbilt University, Nashville, TN (A.R.H., J.H.N.); Cleveland Clinic, OH (G.J.B., M.A.A., J.B., S.A.A.C., S.C.E., B.H., J.K.L., M.A.O., W.H.W.T.); Wayne State University/John D. Dingell VAMC, Detroil, MI (A.A.); Columbia University, New York, NY (E.B.R., W.K.C.); Mayo Clinic, Rochester, MN (B.A.B., R.P.F.); Pulmonary Hypertension Association, Silver Spring, MD (M.P.G.); New York University Medical Center (G.G.); Johns Hopkins Hospital, Baltimore, MD (P.M.H., S.C.M.); Tufts Medical Center, Boston, MA (N.S.H.); Weill Cornell Medicine, New York, NY (E.M.H.); Brigham and Women's Hospital, Boston, MA (B.A.M., D.M.S., A.B.W., J.A.L.); The University of Arizona, Tucson (F.P.R., J.X.-J.Y.); and National Heart, Lung and Blood Institute, Bethesda, MD (L.X.).

    Novel Antithrombotic Drugs on the Horizon: The Ultimate Promise to Prevent Clotting While Avoiding Bleeding.
    Circ Res 2017 Oct;121(10):1133-1135
    From the Atherothrombosis and Vascular Biology Program, Baker Heart and Diabetes Institute, Melbourne, Australia (J.D.M., K.P.); and Department of Medicine (J.D.M., K.P.), Department of Immunology (K.P.), Department of Clinical Haematology, Alfred Hospital (J.D.M.), and Heart Centre, Alfred Hospital (K.P.), Monash University, Melbourne, Australia.

    Attenuation of Myeloid Specific TGFβ Signaling Induces Inflammatory Cerebrovascular Disease and Stroke.
    Circ Res 2017 Oct 19. Epub 2017 Oct 19.
    Laboratory of Cancer Biology and Genetics, NIH.
    Rationale: Cryptogenic strokes, those of unknown cause, have been estimated as high as 30-40% of strokes. Inflammation has been suggested as a critical etiological factor. However, there is lack of experimental evidence. Read More

    Genetic Depletion or Hyperresponsiveness of Natural Killer Cells Do Not Affect Atherosclerosis Development.
    Circ Res 2017 Oct 18. Epub 2017 Oct 18.
    INSERM U970
    Rationale: Chronic inflammation is central in the development of atherosclerosis. Both innate and adaptive immunity are involved. Although several studies have evaluated the functions of NK cells in experimental animal models of atherosclerosis, it is not yet clear whether NK cells behave as protective or pro-atherogenic effectors. Read More

    Cell Type-Specific Chromatin Signatures Underline Regulatory DNA Elements in Human Induced Pluripotent Stem Cells and Somatic Cells.
    Circ Res 2017 Nov 13;121(11):1237-1250. Epub 2017 Oct 13.
    From the Stanford Cardiovascular Institute, Department of Medicine, Division of Cardiology, Institute of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, CA (M.-T.Z., N.-Y.S., N.M., J.L., S.L.Z., J.C.W.); Department of Cardiovascular Surgery of the Frist Affiliated Hospital, Institute for Cardiovascular Science, Soochow University, Suzhou, Jiangsu, China (S.H.); Department of Chemical and Systems Biology, Stanford University School of Medicine, CA (R.S.); and Department of Genetics, Stanford University School of Medicine, CA (F.J., M.P.S.).
    Rationale: Regulatory DNA elements in the human genome play important roles in determining the transcriptional abundance and spatiotemporal gene expression during embryonic heart development and somatic cell reprogramming. It is not well known how chromatin marks in regulatory DNA elements are modulated to establish cell type-specific gene expression in the human heart.

    Objective: We aimed to decipher the cell type-specific epigenetic signatures in regulatory DNA elements and how they modulate heart-specific gene expression. Read More

    General Overview of the 14th International Symposium on Stem Cell Therapy and Cardiovascular Innovations: Working Progress of a Global Initiative in 2017.
    Circ Res 2017 Oct;121(9):1040-1043
    From the Department of Cardiology, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), CIBERCV, Madrid, Spain (R.S.-R., A.M.C., M.E.F.-S., A.V.A., E.G.I., M.E.V.-Á., F.F.-A.); and Universidad Complutense de Madrid, Spain (R.S.-R., M.E.F.-S., A.V.A., E.G.I., M.E.V.-Á., F.F.-A.).

    Current State of Basic and Translational Cardiovascular Research in Spain.
    Circ Res 2017 Oct;121(9):1036-1039
    From the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain (E.L.-P., V.A., V.F., B.I.); CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain (E.L.-P., V.A., F.F.-A., B.I.); National Heart and Lung Institute, Imperial College London, United Kingdom (E.L.-P.); Servicio de Cardiología, Hospital General Universitario Gregorio Marañón, Madrid, Spain (F.F.-A.); The Zena and Michael A. Wiener CVI, Icahn School of Medicine at Mount Sinai, NY (V.F.); and Department of Cardiology, Instituto de Investigación Sanitaria (IIS), Fundación Jiménez Díaz Hospital, Madrid, Spain (B.I.).

    Novel Pathways for Regulation of Sinoatrial Node Plasticity and Heart Rate.
    Circ Res 2017 Oct;121(9):1027-1028
    From the Dorothy M. Davis Heart and Lung Research Institute, College of Medicine (P.J.M., T.J.H.), Department of Physiology & Cell Biology (P.J.M.), Division of Cardiovascular Medicine, Department of Internal Medicine, (P.J.M., T.J.H.), The Ohio State University College of Medicine and Wexner Medical Center, Columbus; and Department of Biomedical Engineering, The Ohio State University College of Engineering & Cell Biology, Columbus (T.J.H.).

    Lactate Promotes Synthetic Phenotype in Vascular Smooth Muscle Cells.
    Circ Res 2017 Nov 11;121(11):1251-1262. Epub 2017 Oct 11.
    From the Division of Cardiology, Department of Medicine (L.Y., T.N., C.J., B.Y.), Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine (A.G., C.H., Z.G.) and Department of Paediatrics (G.R.G.), University of Minnesota Medical School, Minneapolis; Department of Biomedical Engineering, University of Alabama at Birmingham (L.G., J.Z.); and Department of Infectious Disease, Renmin Hospital (J.Y.) and Department of Microbiology, School of Basic Medical Science (J.Y., J.Z.), Hubei University of Medicine, Shiyan, China.
    Rationale: The phenotypes of vascular smooth muscle cells (vSMCs) comprise a continuum bounded by predominantly contractile and synthetic cells. Some evidence suggests that contractile vSMCs can assume a more synthetic phenotype in response to ischemic injury, but the mechanisms that activate this phenotypic switch are poorly understood.

    Objective: To determine whether lactate, which increases in response to regional ischemia, may promote the synthetic phenotype in vSMCs. Read More

    Mitochondrial Cardiomyopathy Caused by Elevated Reactive Oxygen Species and Impaired Cardiomyocyte Proliferation.
    Circ Res 2017 Oct 11. Epub 2017 Oct 11.
    Cardiology, Boston Children's Hospital
    Rationale: Although mitochondrial diseases often cause abnormal myocardial development, the mechanisms by which mitochondria influence heart growth and function are poorly understood. Objective: To investigate these disease mechanisms, we studied a genetic model of mitochondrial dysfunction caused by inactivation of Tfam (Transcription Factor A, Mitochondrial), a nuclear-encoded gene that is essential for mitochondrial gene transcription and mitochondrial DNA replication. Methods and Results:Tfam inactivation by Nkx2. Read More

    CCND2 Overexpression Enhances the Regenerative Potency of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes: Remuscularization of Injured Ventricle.
    Circ Res 2017 Oct 10. Epub 2017 Oct 10.
    Biomedical Engineering, University of Alabama at Birmingham
    Rationale: The effectiveness of transplanted, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) for treatment of ischemic myocardial injury is limited by the exceptionally low engraftment rate. Objective: To determine whether overexpression of the cell-cycle activator CCND2 in hiPSC-CMs can increase the graft size and improve myocardial recovery in a mouse model of myocardial infarction (MI) by increasing the proliferation of grafted cells. Methods and Results: Human CCND2 was delivered to hiPSCs via lenti-viral mediated gene transfection. Read More

    The Trials and Tribulations of CETP Inhibitors.
    Circ Res 2017 Oct 10. Epub 2017 Oct 10.
    Institute for Translational Medicine and Therapeutics, University of Pennsylvania School of Medicine.
    The development of CETP inhibitors has had a long and difficult course with three compounds failing in phase III clinical trials. Finally, the REVEAL trial has shown that the CETP inhibitor anacetrapib decreased coronary heart disease when added to statin therapy. While the result is different to earlier studies, this is likely related to the size and duration of the trial. Read More

    A Distinct Cellular Basis for Early Cardiac Arrhythmias, The Cardinal Manifestation of Arrhythmogenic Cardiomyopathy, and the Skin Phenotype of Cardiocutaneous Syndromes.
    Circ Res 2017 Oct 10. Epub 2017 Oct 10.
    Center for Cardiovascular Genetics, University of Texas Health Sciences Center at Houston
    Rationale: Arrhythmogenic cardiomyopathy (ACM) is caused primarily by mutations in genes encoding desmosome proteins. Ventricular arrhythmias are the cardinal and typically early manifestations, whereas myocardial fibroadiposis is the pathological hallmark. Homozygous DSP (desmoplakin) and JUP (plakoglobin) mutations are responsible for a subset of ACM patients that exhibit cardiac arrhythmias and dysfunction, palmo-planter keratosis, and hair abnormalities (cardiocutaneous syndromes). Read More

    Thyroid and Glucocorticoid Hormones Promote Functional T-tubule Development in Human-Induced Pluripotent Stem Cell Derived Cardiomyocytes.
    Circ Res 2017 Oct 2. Epub 2017 Oct 2.
    Pharmacology, Vanderbilt University Medical Center
    Rationale: Human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CM) are increasingly being used for modeling heart disease and are under development for regeneration of the injured heart. However, incomplete structural and functional maturation of hiPSC-CM including lack of t-tubules, immature excitation-contraction (EC) coupling, and inefficient Ca-induced Ca release (CICR) remain major limitations. Objective: Thyroid and glucocorticoid hormones are critical for heart maturation. Read More

    Safety and Efficacy of the Intravenous Infusion of Umbilical Cord Mesenchymal Stem Cells in Patients With Heart Failure: A Phase 1/2 Randomized Controlled Trial (RIMECARD Trial [Randomized Clinical Trial of Intravenous Infusion Umbilical Cord Mesenchymal Stem Cells on Cardiopathy]).
    Circ Res 2017 Oct 26;121(10):1192-1204. Epub 2017 Sep 26.
    From the Laboratory of Nano-Regenerative Medicine (J.B., P.L.G., F.A.-M., J.C., F.E.F., M.K.) and Department of Internal Medicine (F.J.V., R.E.L., F.E.F.), Faculty of Medicine, Universidad de los Andes, Santiago, Chile; Department of Cardiology, Clínica Santa Maria, Santiago, Chile (J.B., E.A., C.G., R.L., P.A.P., G.V.); Program for Translational Research in Cell Therapy, Clínica Universidad de los Andes, Santiago, Chile (J.B., F.J.V., F.E.F., M.K.); Consorcio Regenero, Chilean Consortium for Regenerative Medicine, Santiago, Chile (P.L.G., F.A., J.C., F.E.F., M.K.); Department of Cardiology, Clínica Davila, Santiago, Chile (R.E.L., P.R., I.P.); Cells for Cells, Santiago, Chile (V.M.L., M.K.); Public Health School, Faculty of Medicine, Universidad de Chile, Santiago, Chile (C.N.); Division of Physical Medicine Rehabilitation, University of Utah, Salt Lake City (M.J.B.); and Department of Surgery, University of Miami School of Medicine, FL (A.N.P.).
    Rationale: Umbilical cord-derived mesenchymal stem cells (UC-MSC) are easily accessible and expanded in vitro, possess distinct properties, and improve myocardial remodeling and function in experimental models of cardiovascular disease. Although bone marrow-derived mesenchymal stem cells have been previously assessed for their therapeutic potential in individuals with heart failure and reduced ejection fraction, no clinical trial has evaluated intravenous infusion of UC-MSCs in these patients.

    Objective: Evaluate the safety and efficacy of the intravenous infusion of UC-MSC in patients with chronic stable heart failure and reduced ejection fraction. Read More

    Calcium-Dependent Arrhythmogenic Foci Created by Weakly Coupled Myocytes in the Failing Heart.
    Circ Res 2017 Oct 2. Epub 2017 Oct 2.
    Pharmacology, University of California, Davis
    Rationale: Intercellular uncoupling and Ca mishandling can initiate triggered ventricular arrhythmias. Spontaneous Ca release activates inward current which depolarizes membrane potential (Vm) and can trigger action potentials in isolated myocytes. However, cell-cell coupling in intact hearts limits local depolarization and may protect hearts from this arrhythmogenic mechanism. Read More

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