Cardiomyocyte-specific overexpression of nitric oxide synthase 3 improves left ventricular performance and reduces compensatory hypertrophy after myocardial infarction. - Wikidata - wikimedia - TriplyDB

Cardiomyocyte-specific overexpression of nitric oxide synthase 3 improves left ventricular performance and reduces compensatory hypertrophy after myocardial infarction.

Cardiomyocyte-specific overexpression of nitric oxide synthase 3 improves left ventricular performance and reduces compensatory hypertrophy after myocardial infarction.

http://www.wikidata.org/entity/Q44814453

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Altered Nitric Oxide System in Cardiovascular and Renal Diseases Interaction of Hydrogen Sulfide with Nitric Oxide in the Cardiovascular System Nitric oxide synthases, S-nitrosylation and cardiovascular health: from molecular mechanisms to therapeutic opportunities (review)Nitric oxide synthases in heart failure Targeting Nitric Oxide with Natural Derived Compounds as a Therapeutic Strategy in Vascular Diseases Neuronal nitric oxide synthase in hypertension - an update Slow progressive conduction and contraction defects in loss of Nkx2-5 mice after cardiomyocyte terminal differentiation Tongxinluo protects against pressure overload-induced heart failure in mice involving VEGF/Akt/eNOS pathway activation Inactivation of Smad5 in endothelial cells and smooth muscle cells demonstrates that Smad5 is required for cardiac homeostasis Displacement-encoded and manganese-enhanced cardiac MRI reveal that nNOS, not eNOS, plays a dominant role in modulating contraction and calcium influx in the mammalian heart.Ventricular phosphodiesterase-5 expression is increased in patients with advanced heart failure and contributes to adverse ventricular remodeling after myocardial infarction in mice.Novel protective role of endogenous cardiac myocyte P2X4 receptors in heart failure Vitamin D is a regulator of endothelial nitric oxide synthase and arterial stiffness in mice Protective effects of nitric oxide synthase 3 and soluble guanylate cyclase on the outcome of cardiac arrest and cardiopulmonary resuscitation in mice.Natakalim improves post-infarction left ventricular remodeling by restoring the coordinated balance between endothelial function and cardiac hypertrophy.Gender differences in adiponectin modulation of cardiac remodeling in mice deficient in endothelial nitric oxide synthase.Impairment of endothelial-myocardial interaction increases the susceptibility of cardiomyocytes to ischemia/reperfusion injury.Regulation of Ryanodine Receptor Ion Channels Through Posttranslational Modifications.Nitric oxide, interorganelle communication, and energy flow: a novel route to slow aging.sGC{alpha}1 mediates the negative inotropic effects of NO in cardiac myocytes independent of changes in calcium handling The effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone on the pressure overload-induced progression of cardiac hypertrophy to cardiac failure.Mechanical and non-mechanical functions of Dystrophin can prevent cardiac abnormalities in Drosophila.Reactive oxygen species in cardiovascular disease.Nitric oxide-cyclic GMP signaling in stem cell differentiation Nitric oxide signaling and the regulation of myocardial function.Cytochrome P450 epoxygenase gene function in hypoxic pulmonary vasoconstriction and pulmonary vascular remodeling Nitric oxide and the heart: update on new paradigms.Regression of pathological cardiac hypertrophy: signaling pathways and therapeutic targets.Modulation of myocardial contraction by peroxynitrite Pathophysiology of hypertension in the absence of nitric oxide/cyclic GMP signaling.The emerging role of neuronal nitric oxide synthase in the regulation of myocardial function.Neuronal nitric oxide synthase is indispensable for the cardiac adaptive effects of exercise.Isosorbide dinitrate-hydralazine combination therapy in African Americans with heart failure Nitric oxide promotes distant organ protection: evidence for an endocrine role of nitric oxide.Future perspectives for the treatment of pulmonary arterial hypertension.Regulation of DDAH1 as a Potential Therapeutic Target for Treating Cardiovascular Diseases.Nitrite therapy improves left ventricular function during heart failure via restoration of nitric oxide-mediated cytoprotective signaling.Isoproterenol-induced heart failure in the rat is associated with nitric oxide-dependent functional alterations of cardiac function.Constitutive nitric oxide synthases in the heart from hypertrophy to failure.Experimental Myocardial Infarction Upregulates Circulating Fibroblast Growth Factor-23.

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P2860

Cardiomyocyte-specific overexpression of nitric oxide synthase 3 improves left ventricular performance and reduces compensatory hypertrophy after myocardial infarction.

http://www.wikidata.org/entity/Q44814453

description

2004 nî lūn-bûn

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2004年の論文

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年學術文章

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2004年學術文章

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name

Cardiomyocyte-specific overexp ...... y after myocardial infarction.

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Cardiomyocyte-specific overexp ...... y after myocardial infarction.

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Cardiomyocyte-specific overexp ...... y after myocardial infarction.

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Cardiomyocyte-specific overexp ...... y after myocardial infarction.

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Circulation Research

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Desire Collen

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Hilde Gillijns

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Kenneth D Bloch

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Luc Schoonjans

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Marc Tjwa

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Marielle Scherrer-Crosbie

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Marijke Pellens

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Peter Jans

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Stefan Janssens

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Zsolt Szelid

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10.1161/01.RES.0000126497.38281.23

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Michael H. Picard

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2004-03-25T00:00:00Z

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