NADPH oxidase-dependent oxidative stress in the failing heart: From pathogenic roles to therapeutic approach

Yanti Octavia, Hans Peter Brunner-La Rocca, An L. Moens*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

56 Citations (Web of Science)


Heart failure (HF) occurs when the adaptation mechanisms of the heart fail to compensate for stress factors, such as pressure overload, myocardial infarction, inflammation, diabetes, and cardiotoxic drugs, with subsequent ventricular hypertrophy, fibrosis, myocardial dysfunction, and chamber dilatation. Oxidative stress, defined as an imbalance between reactive oxygen species (ROS) generation and the capacity of antioxidant defense systems, has been authenticated as a pivotal player in the cardiopathogenesis of the various HF sub-types. The family of NADPH oxidases has been investigated as a key enzymatic source of ROS in the pathogenesis of HF. In this review, we discuss the importance of NADPH oxidase-dependent ROS generation in the various subtypes of HF and its implications. A better understanding of the pathogenic roles of NADPH oxidases in the failing heart is likely to provide novel therapeutic strategies for the prevention and treatment of HF.
Original languageEnglish
Pages (from-to)291-297
JournalFree Radical Biology and Medicine
Issue number2
Publication statusPublished - 15 Jan 2012


  • Heart failure
  • Ventricular remodeling
  • Myocardial dysfunction
  • Reactive oxygen species
  • NADPH oxidases
  • Free radicals

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