Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 52, Issue 9, Pages 1607-1619Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2012.01.025
Keywords
NAD(P)H oxidase; Endothelial cells; Vascular smooth muscle cells; Blood cells; AMPK; Cardiovascular diseases; Free radicals
Funding
- National Institutes of Health RO1 [HL110488, HL105157, HL089920, HL080499, HL079584, HL074399]
- American Diabetes Association
- American Heart Association [11SDG5560036]
- Warren Chair in Diabetes Research of the University of Oklahoma Health Sciences Center
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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are ubiquitously produced in cardiovascular systems. Under physiological conditions, ROS/RNS function as signaling molecules that are essential in maintaining cardiovascular function. Aberrant concentrations of ROS/RNS have been demonstrated in cardiovascular diseases owing to increased production or decreased scavenging, which have been considered common pathways for the initiation and progression of cardiovascular diseases such as atherosclerosis, hypertension, (re)stenosis, and congestive heart failure. NAD(P)H oxidases are primary sources of ROS and can be induced or activated by all known cardiovascular risk factors. Stresses, hormones, vasoactive agents, and cytokines via different signaling cascades control the expression and activity of these enzymes and of their regulatory subunits. But the molecular mechanisms by which NAD(P)H oxidase is regulated in cardiovascular systems remain poorly characterized. Investigations by us and others suggest that adenosine monophosphate-activated protein kinase (AMPK), as an energy sensor and modulator, is highly sensitive to ROS/RNS. We have also obtained convincing evidence that AMPK is a physiological suppressor of NAD(P)H oxidase in multiple cardiovascular cell systems. In this review, we summarize our current understanding of how AMPK functions as a physiological repressor of NAD(P)H oxidase. (c) 2012 Elsevier Inc. All rights reserved.
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