NADPH oxidase and heart failure.
Reactive oxygen species play important roles in the pathophysiology of chronic heart failure secondary to chronic left ventricular hypertrophy or myocardial infarction. Reactive oxygen species influence several components of the phenotype of the failing heart, including contractile function, interstitial fibrosis, endothelial dysfunction and myocyte hypertrophy. Recent studies implicate the production of reactive oxygen species by a family of NADPH oxidases in these effects. NADPH oxidases are activated in an isoform-specific manner by many pathophysiological stimuli and exert distinct downstream effects. Understanding NADPH oxidase activation and regulation, and their downstream effectors, could help to develop novel therapeutic targets.
King's College London, Department of Cardiology, Cardiovascular Division, London SE5 9PJ, UK.
Colin E
CE
Murdoch
David J
DJ
Grieve
Alison C
AC
Cave
Yee Hoo
YH
Looi
Ajay M
AM
Shah
D000818:Animals; D006333:Heart Failure / Q000209:etiology* / Q000378:metabolism; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology*; D009203:Myocardial Infarction / Q000209:etiology*; D019255:NADPH Oxidases / Q000378:metabolism / Q000502:physiology*; D010084:Oxidation-Reduction; D017382:Reactive Oxygen Species / Q000009:adverse effects / Q000378:metabolism / Q000494:pharmacology*
D017382:Reactive Oxygen Species; D019255:NADPH Oxidases