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NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology

Research output: Contribution to journalArticle

A Cave, D Grieve, S Johar, M Zhang, A M Shah

Original languageEnglish
Pages (from-to)2327 - 2334
Number of pages8
JournalPhilosophical Transactions of the Royal Society of London Series B: Biological Sciences
Issue number1464
Publication statusPublished - 29 Dec 2005

King's Authors


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

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