title: NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology.
abstract: Chronic heart failure, secondary to left ventricular hypertrophy or myocardial infarction, is a condition with increasing morbidity and mortality. Although the mechanisms underlying the development and progression of this condition remain a subject of intense interest, there is now growing evidence that redox-sensitive pathways play an important role. This article focuses on the involvement of reactive oxygen species derived from a family of superoxide-generating enzymes, termed NADPH oxidases (NOXs), in the pathophysiology of ventricular hypertrophy, the accompanying interstitial fibrosis and subsequent heart failure. In particular, the apparent ability of the different NADPH oxidase isoforms to define the response of a cell to a range of physiological and pathophysiological stimuli is reviewed. If confirmed, these data would suggest that independently targeting different members of the NOX family may hold the potential for therapeutic intervention in the treatment of cardiac disease.
authors.affiliation: King's College London Cardiovascular Division London SE5 9PJ, UK.
authors.forename: Alison
authors.initials: A
authors.lastname: Cave
authors.forename: David
authors.initials: D
authors.lastname: Grieve
authors.forename: Sofian
authors.initials: S
authors.lastname: Johar
authors.forename: Min
authors.initials: M
authors.lastname: Zhang
authors.forename: Ajay M
authors.initials: AM
authors.lastname: Shah
mesh_terms: D002312:Cardiomyopathy, Hypertrophic / Q000378:metabolism / Q000503:physiopathology*; D004719:Endomyocardial Fibrosis / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism; D019255:NADPH Oxidases / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D007527:Isoenzymes; D017382:Reactive Oxygen Species; D019255:NADPH Oxidases