Scientific Article
previous document  unige:11141  next document
add to browser collection
Title

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

Authors
Published in Physiological Reviews. 2007, vol. 87, no. 1, p. 245-313
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 AnimalsHumansNADPH Oxidase/ physiologyReactive Oxygen Species
Identifiers
PMID: 17237347
Full text
Article - document accessible for UNIGE members only Limited access to UNIGE
Other version: http://physrev.physiology.org/cgi/reprint/87/1/245.pdf
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. https://archive-ouverte.unige.ch/unige:11141

185 hits

0 download

Update

Deposited on : 2010-08-27

Export document
Format :
Citation style :