Crossref journal-article
American Physiological Society
Physiological Reviews (24)
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/gp91phox), 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 actvity 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.

Bibliography

Bedard, K., & Krause, K.-H. (2007). The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology. Physiological Reviews, 87(1), 245–313.

Authors 2
  1. Karen Bedard (first)
  2. Karl-Heinz Krause (additional)
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Dates
Type When
Created 18 years, 7 months ago (Jan. 19, 2007, 1:38 p.m.)
Deposited 7 months, 3 weeks ago (Jan. 12, 2025, 10:03 p.m.)
Indexed 40 minutes ago (Sept. 7, 2025, 2:15 p.m.)
Issued 18 years, 8 months ago (Jan. 1, 2007)
Published 18 years, 8 months ago (Jan. 1, 2007)
Published Print 18 years, 8 months ago (Jan. 1, 2007)
Funders 0

None

@article{Bedard_2007, title={The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology}, volume={87}, ISSN={1522-1210}, url={http://dx.doi.org/10.1152/physrev.00044.2005}, DOI={10.1152/physrev.00044.2005}, number={1}, journal={Physiological Reviews}, publisher={American Physiological Society}, author={Bedard, Karen and Krause, Karl-Heinz}, year={2007}, month=jan, pages={245–313} }