NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology

• Published in: Philosophical transactions of the Royal Society of London. Series B. Biological sciences Vol. 360; no. 1464; pp. 2327 - 2334
• Main Authors: Cave, Alison, Grieve, David, Johar, Sofian, Zhang, Min, Shah, Ajay M
• Format: Journal Article
• Language: English
• Published: London The Royal Society 29.12.2005
• Subjects: Cardiomyopathy, Hypertrophic - metabolism; Cardiomyopathy, Hypertrophic - physiopathology; Endomyocardial Fibrosis - metabolism; Endomyocardial Fibrosis - physiopathology; Fibrosis; Heart; Heart Failure; Humans; Hypertrophy; Isoenzymes - metabolism; Left ventricular hypertrophy; Myocardium; NADPH oxidase; NADPH Oxidases - metabolism; Oxidases; Oxidative Stress; Oxidative Stress - physiology; Protein isoforms; Reactive Oxygen Species; Reactive Oxygen Species - metabolism; Renovations
• ISSN: 0962-8436; 1471-2970
• DOI: 10.1098/rstb.2005.1772

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.