Involvement of NADPH oxidases in cardiac remodelling and heart failure

Alexander Sirker, Min Zhang, Colin Murdoch, Ajay M. Shah

Research output: Contribution to journalArticle

Abstract

Cardiac remodelling occurs in response to stress, such as chronic hypertension or myocardial infarction, and forms the substrate for subsequent development of heart failure. Key pathophysiological features include ventricular hypertrophy, interstitial fibrosis, contractile dysfunction, and chamber dilatation. Although the molecular mechanisms are complex and not fully defined, substantial evidence now implicates increased oxidative stress as being important. The NADPH oxidase ('Nox') enzymes are a particularly important source of reactive oxygen species that are implicated in redox signalling. This article reviews the evidence for an involvement of NADPH oxidases in different aspects of adverse cardiac remodelling. A better understanding of the roles of this complex enzyme family may define novel therapeutic targets for the prevention of heart failure.
Original languageEnglish
Pages (from-to)649-660
Number of pages12
JournalJournal of the American Society of Nephrology
Volume27
Issue number6
DOIs
Publication statusPublished - Oct 2007

Fingerprint

NADPH Oxidase
Heart Failure
Enzymes
Hypertrophy
Oxidation-Reduction
Dilatation
Reactive Oxygen Species
Oxidative Stress
Fibrosis
Myocardial Infarction
Hypertension
Therapeutics

Keywords

  • cardiac hypertrophy
  • cardiac remodelling
  • heart failure
  • NADPH oxidases
  • reactive oxygen species
  • redox signalling

Cite this

Sirker, Alexander ; Zhang, Min ; Murdoch, Colin ; Shah, Ajay M. / Involvement of NADPH oxidases in cardiac remodelling and heart failure. In: Journal of the American Society of Nephrology. 2007 ; Vol. 27, No. 6. pp. 649-660.
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Involvement of NADPH oxidases in cardiac remodelling and heart failure. / Sirker, Alexander; Zhang, Min; Murdoch, Colin; Shah, Ajay M.

In: Journal of the American Society of Nephrology, Vol. 27, No. 6, 10.2007, p. 649-660.

Research output: Contribution to journalArticle

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