NADPH oxidases, reactive oxygen species, and the kidney: friend and foe

Sedeek, M., Nasrallah, R., Touyz, R.M. and Hebert, R.L. (2013) NADPH oxidases, reactive oxygen species, and the kidney: friend and foe. Journal of the American Society of Nephrology, 24(10), pp. 1512-1518. (doi: 10.1681/ASN.2012111112)

Full text not currently available from Enlighten.

Abstract

Reactive oxygen species (ROS) play an important role in normal cellular physiology. They regulate different biologic processes such as cell defense, hormone synthesis and signaling, activation of G protein-coupled receptors, and ion channels and kinases/phosphatases. ROS are also important regulators of transcription factors and gene expression. On the other hand, in pathologic conditions, a surplus of ROS in tissue results in oxidative stress with various injurious consequences such as inflammation and fibrosis. NADPH oxidases are one of the many sources of ROS in biologic systems, and there are seven isoforms (Nox1–5, Duox1, Duox2). Nox4 is the predominant form in the kidney, although Nox2 is also expressed. Nox4 has been implicated in the basal production of ROS in the kidney and in pathologic conditions such as diabetic nephropathy and CKD; upregulation of Nox4 may be important in renal oxidative stress and kidney injury. Although there is growing evidence indicating the involvement of NADPH oxidase in renal pathology, there is a paucity of information on the role of NADPH oxidase in the regulation of normal renal function. Here we provide an update on the role of NADPH oxidases and ROS in renal physiology and pathology.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Touyz, Professor Rhian
Authors: Sedeek, M., Nasrallah, R., Touyz, R.M., and Hebert, R.L.
College/School:College of Medical Veterinary and Life Sciences > School of Cardiovascular & Metabolic Health
Journal Name:Journal of the American Society of Nephrology
ISSN:1046-6673
ISSN (Online):1533-3450

University Staff: Request a correction | Enlighten Editors: Update this record