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HERO ID
2837738
Reference Type
Journal Article
Title
Vascular oxidative stress, nitric oxide and atherosclerosis
Author(s)
Li, H; Horke, S; Förstermann, U
Year
2014
Is Peer Reviewed?
Yes
Journal
Atherosclerosis
ISSN:
0021-9150
EISSN:
1879-1484
Volume
237
Issue
1
Page Numbers
208-219
Language
English
PMID
25244505
DOI
10.1016/j.atherosclerosis.2014.09.001
Web of Science Id
WOS:000345011300034
Abstract
In the vascular wall, reactive oxygen species (ROS) are produced by several enzyme systems including NADPH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase (eNOS) and the mitochondrial electron transport chain. On the other hand, the vasculature is protected by antioxidant enzyme systems, including superoxide dismutases, catalase, glutathione peroxidases and paraoxonases, which detoxify ROS. Cardiovascular risk factors such as hypercholesterolemia, hypertension, and diabetes mellitus enhance ROS generation, resulting in oxidative stress. This leads to oxidative modification of lipoproteins and phospholipids, mechanisms that contribute to atherogenesis. In addition, oxidation of tetrahydrobiopterin may cause eNOS uncoupling and thus potentiation of oxidative stress and reduction of eNOS-derived NO, which is a protective principle in the vasculature. This review summarizes the latest advances in the role of ROS-producing enzymes, antioxidative enzymes as well as NO synthases in the initiation and development of atherosclerosis.
Keywords
Reactive oxygen species; Oxidative stress; Nitric oxide; Atherosclerosis
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