NOX1, 2, 4, 5: counting out oxidative stress

K. Wingler, J. J. R. Hermans, P. Schiffers, A. L. Moens, M. Paul, H. H. H. W. Schmidt*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


For decades, oxidative stress has been discussed as a key mechanism of endothelial dysfunction and cardiovascular disease. However, attempts to validate and exploit this hypothesis clinically by supplementing antioxidants have failed. Nevertheless, this does not disprove the oxidative stress hypothesis. As a certain degree of reactive oxygen species (ROS) formation appears to be physiological and beneficial. To reduce oxidative stress therapeutically, two alternative approaches are being developed. One is the repair of key signalling components that are compromised by oxidative stress. These include uncoupled endothelial nitric oxide (NO) synthase and oxidized/heme-free NO receptor soluble guanylate cyclase. A second approach is to identify and effectively inhibit the relevant source(s) of ROS in a given disease condition. A highly likely target in this context is the family of NADPH oxidases. Animal models, including NOX knockout mice and new pharmacological inhibitors of NADPH oxidases have opened up a new era of oxidative stress research and have paved the way for new cardiovascular therapies.
Original languageEnglish
Pages (from-to)866-883
JournalBritish Journal of Pharmacology
Issue number3
Publication statusPublished - Oct 2011


  • endothelial dysfunction
  • NADPH oxidases
  • NOX
  • cardiovascular diseases
  • NADPH oxidase inhibitors


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