NADPH oxidase and heart failure

Colin E. Murdoch, David J. Grieve, Alison C. Cave, Yee Hoo Looi, Ajay M. Shah

Research output: Contribution to journalArticle

Abstract

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.
Original languageEnglish
Pages (from-to)148-153
Number of pages6
JournalCurrent Opinion in Pharmacology
Volume6
Issue number2
Early online date17 Feb 2006
DOIs
Publication statusPublished - Apr 2006

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    Murdoch, C. E., Grieve, D. J., Cave, A. C., Looi, Y. H., & Shah, A. M. (2006). NADPH oxidase and heart failure. Current Opinion in Pharmacology, 6(2), 148-153. https://doi.org/10.1016/j.coph.2005.10.008