NADPH oxidase and heart failure

被引：52

作者：

Murdoch, CE ^{[1
]}

Grieve, DJ ^{[1
]}

Cave, AC ^{[1
]}

Looi, YH ^{[1
]}

Shah, AM ^{[1
]}

机构：

[1] Kings Coll London, Dept Cardiol, Div Cardiovasc, London SE5 9PJ, England

来源：

CURRENT OPINION IN PHARMACOLOGY | 2006年 / 6卷 / 02期

关键词：

D O I：

10.1016/j.coph.2005.10.008

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

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.

引用

页码：148 / 153

页数：6

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