Exploiting cGMP-based therapies for the prevention of left ventricular hypertrophy: NO* and beyond.
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Asymmetric Dimethylarginine Is a Well Established Mediating Risk Factor for Cardiovascular Morbidity and Mortality-Should Patients with Elevated Levels Be Supplemented with Citrulline?Nitroxyl (HNO) stimulates soluble guanylyl cyclase to suppress cardiomyocyte hypertrophy and superoxide generation.Omega-3 fatty acids prevent pressure overload-induced cardiac fibrosis through activation of cyclic GMP/protein kinase G signaling in cardiac fibroblasts.Aging of the nitric oxide system: are we as old as our NO?The soluble guanylyl cyclase activator bay 58-2667 selectively limits cardiomyocyte hypertrophy.Cardiac oxidative stress in a mouse model of neutral lipid storage disease.Low intrinsic exercise capacity in rats predisposes to age-dependent cardiac remodeling independent of macrovascular function.The concomitant coronary vasodilator and positive inotropic actions of the nitroxyl donor Angeli's salt in the intact rat heart: contribution of soluble guanylyl cyclase-dependent and -independent mechanisms.Molecular and cellular basis for diastolic dysfunction.The role of cGMP in the physiological and molecular responses of the right ventricle to pressure overload.New Insights Into Diastolic Dysfunction and Heart Failure With Preserved Ejection Fraction.Targeting vascular (endothelial) dysfunction.Stem cells and diabetic cardiomyopathy: from pathology to therapy.ω3-Polyunsaturated fatty acids for heart failure: Effects of dose on efficacy and novel signaling through free fatty acid receptor 4.Pathophysiological Fundamentals of Diabetic Cardiomyopathy.Protein kinase g iα inhibits pressure overload-induced cardiac remodeling and is required for the cardioprotective effect of sildenafil in vivo.Chronic intratracheal application of the soluble guanylyl cyclase stimulator BAY 41-8543 ameliorates experimental pulmonary hypertension.Unexpected anti-hypertrophic responses to low-level stimulation of protease-activated receptors in adult rat cardiomyocytes.HNO/cGMP-dependent antihypertrophic actions of isopropylamine-NONOate in neonatal rat cardiomyocytes: potential therapeutic advantages of HNO over NO.Attenuating effects of dihydromyricetin on angiotensin II-induced rat cardiomyocyte hypertrophy related to antioxidative activity in a NO-dependent manner.C33(S), a novel PDE9A inhibitor, protects against rat cardiac hypertrophy through upregulating cGMP signaling.3',5'-cIMP as Potential Second Messenger in the Vascular Wall.Enhanced phosphoinositide 3-kinase(p110α) activity prevents diabetes-induced cardiomyopathy and superoxide generation in a mouse model of diabetes.Diabetic Cardiomyopathy: Current and Future Therapies. Beyond Glycemic Control
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P2860
Exploiting cGMP-based therapies for the prevention of left ventricular hypertrophy: NO* and beyond.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
@pt
bilimsel makale
@tr
scientific article published on 29 August 2009
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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
Exploiting cGMP-based therapie ...... r hypertrophy: NO* and beyond.
@en
Exploiting cGMP-based therapie ...... r hypertrophy: NO* and beyond.
@nl
type
label
Exploiting cGMP-based therapie ...... r hypertrophy: NO* and beyond.
@en
Exploiting cGMP-based therapie ...... r hypertrophy: NO* and beyond.
@nl
prefLabel
Exploiting cGMP-based therapie ...... r hypertrophy: NO* and beyond.
@en
Exploiting cGMP-based therapie ...... r hypertrophy: NO* and beyond.
@nl
P2093
P1476
Exploiting cGMP-based therapie ...... ar hypertrophy: NO* and beyond
@en
P2093
Anke C Rosenkranz
Barbara K Kemp-Harper
Igor R Wendt
Jennifer C Irvine
Ruchi Patel
P304
P356
10.1016/J.PHARMTHERA.2009.08.001
P577
2009-08-29T00:00:00Z