about
Adenosine kinase regulation of cardiomyocyte hypertrophy.Genomic profiling of the human heart before and after mechanical support with a ventricular assist device reveals alterations in vascular signaling networks.Adenosine A3 receptor deficiency exerts unanticipated protective effects on the pressure-overloaded left ventricleVascular endothelial-specific dimethylarginine dimethylaminohydrolase-1-deficient mice reveal that vascular endothelium plays an important role in removing asymmetric dimethylarginine.Metformin protects against systolic overload-induced heart failure independent of AMP-activated protein kinase α2.Disruption of sarcolemmal ATP-sensitive potassium channel activity impairs the cardiac response to systolic overload.Oxidative stress regulates left ventricular PDE5 expression in the failing heartEndoplasmic reticulum stress sensor protein kinase R-like endoplasmic reticulum kinase (PERK) protects against pressure overload-induced heart failure and lung remodeling.Loss of AMPK exacerbates experimental autoimmune encephalomyelitis disease severity.Dimethylarginine dimethylaminohydrolase 1 modulates endothelial cell growth through nitric oxide and AktMicrotubule Actin Cross-linking Factor 1 regulates cardiomyocyte microtubule distribution and adaptation to hemodynamic overload.DDAH1 deficiency attenuates endothelial cell cycle progression and angiogenesis.Exacerbated pulmonary arterial hypertension and right ventricular hypertrophy in animals with loss of function of extracellular superoxide dismutase.AMP activated protein kinase-α2 regulates expression of estrogen-related receptor-α, a metabolic transcription factor related to heart failure development.Left ventricular failure produces profound lung remodeling and pulmonary hypertension in mice: heart failure causes severe lung diseaseAMP-activated protein kinase α1 protects against diet-induced insulin resistance and obesity.Inducible nitric oxide synthase deficiency protects the heart from systolic overload-induced ventricular hypertrophy and congestive heart failure.Extracellular superoxide dismutase protects the heart against oxidative stress and hypertrophy after myocardial infarction.Ecto-5'-nucleotidase deficiency exacerbates pressure-overload-induced left ventricular hypertrophy and dysfunction.AMPK attenuates microtubule proliferation in cardiac hypertrophyXanthine oxidase inhibition with febuxostat attenuates systolic overload-induced left ventricular hypertrophy and dysfunction in miceRole of interferon regulatory factor 4 in the regulation of pathological cardiac hypertrophyNADPH oxidase contributes to coronary endothelial dysfunction in the failing heartAdenosine regulation of microtubule dynamics in cardiac hypertrophyLoss of the eukaryotic initiation factor 2α kinase general control nonderepressible 2 protects mice from pressure overload-induced congestive heart failure without affecting ventricular hypertrophy.Genetic and Pharmacologic Inhibition of the Chemokine Receptor CXCR2 Prevents Experimental Hypertension and Vascular Dysfunction.AMP activated protein kinase-alpha2 deficiency exacerbates pressure-overload-induced left ventricular hypertrophy and dysfunction in mice.Inducible nitric oxide synthase inhibits oxygen consumption in collateral-dependent myocardiumToll-interacting protein (Tollip) negatively regulates pressure overload-induced ventricular hypertrophy in miceDouble-stranded RNA-dependent protein kinase deficiency protects the heart from systolic overload-induced congestive heart failure.S-nitrosylation of PDE5 increases its ubiquitin-proteasomal degradation.Role of bone marrow-derived CD11c+ dendritic cells in systolic overload-induced left ventricular inflammation, fibrosis and hypertrophy.CD28/B7 Deficiency Attenuates Systolic Overload-Induced Congestive Heart Failure, Myocardial and Pulmonary Inflammation, and Activated T Cell Accumulation in the Heart and Lungs.Delayed treatment effects of xanthine oxidase inhibition on systolic overload-induced left ventricular hypertrophy and dysfunctionPGC-1 alpha regulates expression of myocardial mitochondrial antioxidants and myocardial oxidative stress after chronic systolic overload.Reduced expression of mitochondrial electron transport chain proteins from hibernating hearts relative to ischemic preconditioned hearts in the second window of protection.Repetitive ischemia increases myocardial dimethylarginine dimethylaminohydrolase 1 expression.Increased extravascular forces limit endothelium-dependent and -independent coronary vasodilation in congestive heart failure.Nitric oxide modulates myocardial oxygen consumption in the failing heart.Adenosine: a modulator of the cardiac response to stress.
P50
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P50
description
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Yingjie Chen
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Yingjie Chen
@en
Yingjie Chen
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Yingjie Chen
@nl
Yingjie Chen
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type
label
Yingjie Chen
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Yingjie Chen
@en
Yingjie Chen
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Yingjie Chen
@nl
Yingjie Chen
@sl
prefLabel
Yingjie Chen
@ast
Yingjie Chen
@en
Yingjie Chen
@es
Yingjie Chen
@nl
Yingjie Chen
@sl
P106
P1153
35271262500
P31
P496
0000-0002-4059-7847