en
Scientific article
English

The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology

Published inPhysiological reviews, vol. 87, no. 1, p. 245-313
Publication date2007
Abstract

For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phagocyte NADPH oxidase were found: NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2. Together with the phagocyte NADPH oxidase itself (NOX2/gp91(phox)), the homologs are now referred to as the NOX family of NADPH oxidases. These enzymes share the capacity to transport electrons across the plasma membrane and to generate superoxide and other downstream reactive oxygen species (ROS). Activation mechanisms and tissue distribution of the different members of the family are markedly different. The physiological functions of NOX family enzymes include host defense, posttranlational processing of proteins, cellular signaling, regulation of gene expression, and cell differentiation. NOX enzymes also contribute to a wide range of pathological processes. NOX deficiency may lead to immunosuppresion, lack of otoconogenesis, or hypothyroidism. Increased NOX activity also contributes to a large number or pathologies, in particular cardiovascular diseases and neurodegeneration. This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.

Keywords
  • Animals
  • Humans
  • NADPH Oxidase/ physiology
  • Reactive Oxygen Species
Affiliation Not a UNIGE publication
Citation (ISO format)
BEDARD, Karen, KRAUSE, Karl-Heinz. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. In: Physiological reviews, 2007, vol. 87, n° 1, p. 245–313. doi: 10.1152/physrev.00044.2005
Main files (1)
Article
accessLevelRestricted
Identifiers
ISSN of the journal0031-9333
1151views
0downloads

Technical informations

Creation2010/08/27 13:33:54
First validation2010/08/27 13:33:54
Update time2023/03/14 16:02:36
Status update2023/03/14 16:02:36
Last indexation2024/02/12 19:14:31
All rights reserved by Archive ouverte UNIGE and the University of GenevaunigeBlack