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Atherosclerosis. 2014 Nov;237(1):208-19. doi: 10.1016/j.atherosclerosis.2014.09.001. Epub 2014 Sep 9.

Vascular oxidative stress, nitric oxide and atherosclerosis.

Author information

1
Department of Pharmacology, Johannes Gutenberg University Medical Center, 55131 Mainz, Germany.
2
Department of Pharmacology, Johannes Gutenberg University Medical Center, 55131 Mainz, Germany. Electronic address: ulrich.forstermann@uni-mainz.de.

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:

Atherosclerosis; Nitric oxide; Oxidative stress; Reactive oxygen species

[Indexed for MEDLINE]

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