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NADPH oxidase-dependent redox signalling in cardiac hypertrophy, remodelling and failure

Research output: Contribution to journalLiterature review

C E Murdoch, M Zhang, A C Cave, A M Shah

Original languageEnglish
Pages (from-to)208 - 215
Number of pages8
JournalCardiovascular Research
Issue number2
Publication statusPublished - 15 Jul 2006

King's Authors


Markers of increased oxidative stress are known to be elevated following acute myocardial infarction and in the context of chronic left ventricular hypertrophy or heart failure, and their levels may correlate with the degree of contractile dysfunction or cardiac deficit. An obvious pathological mechanism that may account for this correlation is the potential deleterious effects of increased oxidative stress through the induction of cellular dysfunction, energetic deficit or cell death. However, reactive oxygen species have several much more subtle effects in the remodelling or failing heart that involve specific redox-regulated modulation of signalling pathways and gene expression. Such redoxsensitive regulation appears to play important roles in the development of several components of the phenotype of the failing heart, for example cardiomyocyte hypertrophy, interstitial fibrosis and chamber remodelling. In this article, we review the evidence supporting the involvement of reactive oxygen species and redox signalling pathways in the development of cardiac hypertrophy and heart failure, with a particular focus on the NADPH oxidase family of superoxide-generating enzymes which appear to be especially important in redox signalling. (c) 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved

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