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Emerging role of oxidative stress in metabolic syndrome and cardiovascular diseases: important role of Rac/ NADPH oxidase
Author(s) -
Elnakish Mohammad T,
Hassanain Hamdy H,
Janssen Paul M,
Angelos Mark G,
Khan Mahmood
Publication year - 2013
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.4255
Subject(s) - nadph oxidase , oxidative stress , nox1 , reactive oxygen species , p22phox , microbiology and biotechnology , oxidative phosphorylation , biochemistry , biology , chemistry
'Oxidative stress' is a term defining states of elevated reactive oxygen species ( ROS ) levels. Normally, ROS control several physiological processes, such as host defence, biosynthesis of hormones, fertilization and cellular signalling. However, oxidative stress has been involved in different pathologies, including metabolic syndrome and numerous cardiovascular diseases. A major source of ROS involved in both metabolic syndrome and cardiovascular pathophysiology is the NADPH oxidase ( NOX ) family of enzymes. NOX is a multi‐component enzyme complex that consists of membrane‐bound cytochrome b ‐558, which is a heterodimer of gp91 phox and p22 phox , cytosolic regulatory subunits p47 phox and p67 phox , and the small GTP ‐binding protein Rac1. Rac1 plays many important biological functions in cells, but perhaps the most unique function of Rac1 is its ability to bind and activate the NOX complex. Furthermore, Rac1 has been reported to be a key regulator of oxidative stress through its co‐regulatory effects on both nitric oxide ( NO ) synthase and NOX . Therefore, the main goal of this review is to give a brief outline about the important role of the Rac1– NOX axis in the pathophysiology of both metabolic syndrome and cardiovascular disease. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.