INDIGO Home University of Illinois at Urbana-Champaign logo uic building uic pavilion uic student center

Redox regulation of Nox proteins

Show simple item record

Bookmark or cite this item: http://hdl.handle.net/10027/7364

Files in this item

File Description Format
PDF Srikanth_review_INDIGO-1.pdf (329KB) (no description provided) PDF
Title: Redox regulation of Nox proteins
Author(s): Pendyala, Srikanth; Natarajan, Viswanathan
Subject(s): NADPH Oxidase ROS endothelium nox proteins
Abstract: The generation of reactive oxygen species (ROS) plays a major role in endothelial signaling and function. Of the several potential sources of ROS in the vasculature, the endothelial NADPH Oxidase (Nox) family of proteins, Nox1, Nox2, Nox4 and Nox5, are major contributors of ROS. Excess generation of ROS contributes to the development and progression of vascular disease. While hyperoxia stimulates ROS production through Nox proteins, hypoxia appears to involve mitochondrial electron transport in the generation of superoxide. ROS generated from Nox proteins and mitochondria are important for oxygen sensing mechanisms. Physiological concentrations of ROS function as signaling molecule in the endothelium; however, excess ROS production leads to pathological disorders like inflammation, atherosclerosis, and lung injury. Regulation of Nox proteins is unclear; however, antioxidants, MAP Kinases, STATs, and Nrf2 regulate Nox under normal physiological and pathological conditions. Studies related to redox regulation of Nox should provide a better understanding of ROS and its role in the pathophysiology of vascular diseases.
Issue Date: 2010-12-31
Publisher: Elsevier
Citation Info: Pendyala, S. & Natarajan, V. 2010. Redox regulation of Nox proteins. Respiratory Physiology and Neurobiology. DOI: 10.1016/j.resp.2010.09.016
Type: Article
Description: Post print version of article may differ from published version. The definitive version is available through Elsevier at DOI: 10.1016/j.resp.2010.09.016
URI: http://hdl.handle.net/10027/7364
ISSN: 1878-1519
Sponsor: NIH RO1 HL 085553 and PO1 HL58064 to V.N
Date Available in INDIGO: 2011-03-01
 

This item appears in the following Collection(s)

Show simple item record

Statistics

Country Code Views
United States of America 142
China 38
United Kingdom 15
Netherlands 8
Germany 4

Browse

My Account

Information

Access Key