about
Coordinated regulation of cardiac Na(+)/Ca (2+) exchanger and Na (+)-K (+)-ATPase by phospholemman (FXYD1)GRK2 in the heart: a GPCR kinase and beyondEpigenetic upregulation of endogenous VEGF-A reduces myocardial infarct size in miceParoxetine Is a Direct Inhibitor of G Protein-Coupled Receptor Kinase 2 and Increases Myocardial ContractilityS100A1 is released from ischemic cardiomyocytes and signals myocardial damage via Toll-like receptor 4Loss of cadherin-binding proteins β-catenin and plakoglobin in the heart leads to gap junction remodeling and arrhythmogenesisCardiac S100A1 protein levels determine contractile performance and propensity toward heart failure after myocardial infarctionS100A1 gene therapy preserves in vivo cardiac function after myocardial infarctionStable myocardial-specific AAV6-S100A1 gene therapy results in chronic functional heart failure rescueTumor necrosis factor-α and lymphotoxin-α mediate myocardial ischemic injury via TNF receptor 1, but are cardioprotective when activating TNF receptor 2Toll-like receptor 9-activation during onset of myocardial ischemia does not influence infarct extensionGSK-3alpha directly regulates beta-adrenergic signaling and the response of the heart to hemodynamic stress in micePhospholemman and beta-adrenergic stimulation in the heart.G protein-coupled receptor kinase 2 ablation in cardiac myocytes before or after myocardial infarction prevents heart failure.Adiponectin: an indispensable molecule in rosiglitazone cardioprotection following myocardial infarction.Cardiomyocyte-derived adiponectin is biologically active in protecting against myocardial ischemia-reperfusion injury.Gi proteins mediate activation of the canonical hedgehog pathway in the myocardium.Reduction of sympathetic activity via adrenal-targeted GRK2 gene deletion attenuates heart failure progression and improves cardiac function after myocardial infarctionGlycogen synthase kinase-3beta regulates post-myocardial infarction remodeling and stress-induced cardiomyocyte proliferation in vivoCardiomyocyte-specific deletion of Gsk3α mitigates post-myocardial infarction remodeling, contractile dysfunction, and heart failure.Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarctionLevel of G protein-coupled receptor kinase-2 determines myocardial ischemia/reperfusion injury via pro- and anti-apoptotic mechanisms.A novel and efficient model of coronary artery ligation and myocardial infarction in the mouse.Phospholemman: a novel cardiac stress protein.Simultaneous administration of insulin-like growth factor-1 and darbepoetin alfa protects the rat myocardium against myocardial infarction and enhances angiogenesisNuclear translocation of cardiac G protein-Coupled Receptor kinase 5 downstream of select Gq-activating hypertrophic ligands is a calmodulin-dependent process.GRK5-mediated exacerbation of pathological cardiac hypertrophy involves facilitation of nuclear NFAT activity.Myocardial Ablation of G Protein-Coupled Receptor Kinase 2 (GRK2) Decreases Ischemia/Reperfusion Injury through an Anti-Intrinsic Apoptotic PathwayAlpha-catenins control cardiomyocyte proliferation by regulating Yap activity.Inhibition of Fas-associated death domain-containing protein (FADD) protects against myocardial ischemia/reperfusion injury in a heart failure mouse modelInhibition of the cardiomyocyte-specific kinase TNNI3K limits oxidative stress, injury, and adverse remodeling in the ischemic heartVitamin D receptor activation protects against myocardial reperfusion injury through inhibition of apoptosis and modulation of autophagyCa²⁺ entry via Trpm2 is essential for cardiac myocyte bioenergetics maintenance.Glycogen synthase kinase-3α limits ischemic injury, cardiac rupture, post-myocardial infarction remodeling and death.G-protein-coupled receptor kinase 2-mediated desensitization of adiponectin receptor 1 in failing heart.Myocardial injury after ischemia-reperfusion in mice deficient in Akt2 is associated with increased cardiac macrophage densityLin28a protects against cardiac ischaemia/reperfusion injury in diabetic mice through the insulin-PI3K-mTOR pathway.Oncostatin M (OSM) protects against cardiac ischaemia/reperfusion injury in diabetic mice by regulating apoptosis, mitochondrial biogenesis and insulin sensitivity.Gi-biased β2AR signaling links GRK2 upregulation to heart failure.Consequence of the tumor-associated conversion to cyclin D1b
P50
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P50
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onderzoeker
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Erhe Gao
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Erhe Gao
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Erhe Gao
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Erhe Gao
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type
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Erhe Gao
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Erhe Gao
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Erhe Gao
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Erhe Gao
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Erhe Gao
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Erhe Gao
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Erhe Gao
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Erhe Gao
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