Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure. - Wikidata - wikimedia - TriplyDB

Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure.

Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure.

http://www.wikidata.org/entity/Q37676218

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Modulation of cardiac contractility by the phospholamban/SERCA2a regulatome Review of novel therapeutic targets for improving heart failure treatment based on experimental and clinical studies Prospects for gene transfer for clinical heart failure Cardiomyocyte protein trafficking: Relevance to heart disease and opportunities for therapeutic intervention Cardiovascular gene therapy for myocardial infarction Alterations in T-tubule and dyad structure in heart disease: challenges and opportunities for computational analyses Molecular targets in heart failure gene therapy: current controversies and translational perspectives 17ß-Estradiol regulates mTORC2 sensitivity to rapamycin in adaptive cardiac remodeling Maturing human pluripotent stem cell-derived cardiomyocytes in human engineered cardiac tissues Expression of sarco (endo) plasmic reticulum calcium ATPase (SERCA) system in normal mouse cardiovascular tissues, heart failure and atherosclerosis Myocardial gene transfer: routes and devices for regulation of transgene expression by modulation of cellular permeability Patient-specific induced pluripotent stem cells as a model for familial dilated cardiomyopathy.AAV's anatomy: roadmap for optimizing vectors for translational success Engineering liver-detargeted AAV9 vectors for cardiac and musculoskeletal gene transfer.SERCA2a gene transfer enhances eNOS expression and activity in endothelial cells.SERCA2a gene therapy can improve symptomatic heart failure in δ-sarcoglycan-deficient animals.Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity.Epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.Neonatal gene transfer of Serca2a delays onset of hypertrophic remodeling and improves function in familial hypertrophic cardiomyopathy.Role of ER stress in ventricular contractile dysfunction in type 2 diabetes Synthetic phosphopeptides enable quantitation of the content and function of the four phosphorylation states of phospholamban in cardiac muscle The interface between monitoring and physiology at the bedside.Attenuation of endoplasmic reticulum stress-related myocardial apoptosis by SERCA2a gene delivery in ischemic heart disease.Hypoxia. 4. Hypoxia and ion channel function Endoplasmic reticulum Ca(2+) handling in excitable cells in health and disease SERCA2a gene transfer improves electrocardiographic performance in aged mdx mice Targeting cardiomyocyte Ca2+ homeostasis in heart failure.BIN1 is reduced and Cav1.2 trafficking is impaired in human failing cardiomyocytes.Exercise training restores the cardiac microRNA-1 and -214 levels regulating Ca2+ handling after myocardial infarction.Protein-protein interactions in calcium transport regulation probed by saturation transfer electron paramagnetic resonance.BATMAN-TCM: a Bioinformatics Analysis Tool for Molecular mechANism of Traditional Chinese Medicine.Cardiac surgical delivery of the sarcoplasmic reticulum calcium ATPase rescues myocytes in ischemic heart failure Bendavia restores mitochondrial energy metabolism gene expression and suppresses cardiac fibrosis in the border zone of the infarcted heart.Therapeutic efficacy of AAV1.SERCA2a in monocrotaline-induced pulmonary arterial hypertension.Luteolin improves cardiac dysfunction in heart failure rats by regulating sarcoplasmic reticulum Ca2+-ATPase 2a.Gene therapy strategies for cardiac electrical dysfunction.Targeted gene therapy for the treatment of heart failure.Pharmacologic and genetic strategies to enhance cell therapy for cardiac regeneration.Calcium cycling proteins and their association with heart failure.Molecular targets of current and prospective heart failure therapies.

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Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure.

http://www.wikidata.org/entity/Q37676218

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on January 2010

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Sarcoplasmic reticulum Ca

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Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure.

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type

label

Sarcoplasmic reticulum Ca

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Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure.

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prefLabel

Sarcoplasmic reticulum Ca

@nl

Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure.

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Expert Opinion on Biological Therapy

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Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure.

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Anne-Marie Lompre

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Elie R Chemaly

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Lahouaria Hadri

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Roger J Hajjar

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P2860

Restoration of contractile function in isolated cardiomyocytes from failing human hearts by gene transfer of SERCA2a.

Heart Disease and Stroke Statistics--2008 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee

A mutation in the human phospholamban gene, deleting arginine 14, results in lethal, hereditary cardiomyopathy.

Targeted disruption of NFATc3, but not NFATc4, reveals an intrinsic defect in calcineurin-mediated cardiac hypertrophic growth

Direct interaction and reciprocal regulation between ASK1 and calcineurin-NFAT control cardiomyocyte death and growth

Cardiac adenoviral S100A1 gene delivery rescues failing myocardium

Stable myocardial-specific AAV6-S100A1 gene therapy results in chronic functional heart failure rescue

Improvement in survival and cardiac metabolism after gene transfer of sarcoplasmic reticulum Ca(2+)-ATPase in a rat model of heart failure

Regulation of cardiac hypertrophy by intracellular signalling pathways

Successful transduction of liver in hemophilia by AAV-Factor IX and limitations imposed by the host immune response

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