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NADPH oxidase and heart failure

Research output: Contribution to journalLiterature review

C E Murdoch, D J Grieve, A C Cave, Y H Looi, A M Shah

Original languageEnglish
Pages (from-to)148 - 153
Number of pages6
JournalCurrent Opinion in Pharmacology
Issue number2
Publication statusPublished - Apr 2006

King's Authors

Research Groups

  • King's College London


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

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