Increased myocardial NADPH oxidase activity in human heart failure.

By C. Heymes, J. Bendall, P. Ratajczak, A. Cave, J. Samuel, G. Hasenfuss, A. Shah. Journal of the American College of Cardiology, 2003

604 citations recorded by the source corpus.

How researchers see this paper

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Reactive Oxygen Species in Cardiovascular Disease (2011, background): “NADPH oxidase activity in myocardium is increased in the failing human hearts [271] and electroparamagnetic resonance studies with spin trapping directly demonstrate an increased levels of O2 in human failing hearts [272].”
Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart (2005, background): “Increased generation of radical oxygen species in response to regional ischemia and depressed myocardial function could activate oxidant-sensitive inflammatory signals in visceral adipose tissue in adjacent adipose stores”
NADPH Oxidases in Cardiovascular Health and Disease (2006, positive): “The knowledge that increased oxidative stress plays important roles in the pathophysiology of many cardiovascular disorders has naturally led to consideration of the potential therapeutic benefit of antioxidant agents.”
Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “Stimuli that may be important in activating NADPH oxidase in cardiac hypertrophy and heart failure include angiotensin II, ET-1, cytokines, and mechanical forces (60).”
NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart (2010, background): “Activation of Nox was also observed in human heart failure, as evidenced by enhanced p47 staining in the sarcolemmal membrane (11).”