Journal ArticleDOI
Oxidative stress in vascular disease and its pharmacological prevention
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TLDR
Molecular mechanisms involved in the induction of oxidative stress under pathological conditions as well as pharmacological approaches (and their molecular mechanisms) are summarized in this review.About:
This article is published in Trends in Pharmacological Sciences.The article was published on 2013-06-01. It has received 263 citations till now. The article focuses on the topics: Oxidative stress & Superoxide dismutase.read more
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Journal ArticleDOI
Roles of Vascular Oxidative Stress and Nitric Oxide in the Pathogenesis of Atherosclerosis
TL;DR: Prevention of vascular oxidative stress and improvement of endothelial NO production represent reasonable therapeutic strategies in addition to the treatment of established risk factors (hypercholesterolemia, hypertension, and diabetes mellitus).
Journal ArticleDOI
Oxidative Stress in Atherosclerosis.
TL;DR: The role of ROS and anti-oxidant mechanisms in the development and progression of atherosclerosis, the role of oxidized low-density lipoprotein cholesterol, and potential anti-Oxidant therapeutic strategies relevant to Atherosclerosis are discussed.
Journal ArticleDOI
Vascular oxidative stress, nitric oxide and atherosclerosis
TL;DR: 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.
Journal ArticleDOI
The role of oxidative stress during inflammatory processes
TL;DR: This article reviews in detail the current knowledge on the fundamental connections between oxidative stress and inflammatory processes, with a special emphasis on the danger molecule high-mobility group box-1, the TLRs, the NLRP-3 receptor, and the inflammasome, as well as the transcription factor nuclear factor-κB.
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Antioxidant effects of resveratrol in the cardiovascular system
TL;DR: The antioxidant effects of resveratrol (3,5,4'‐trihydroxy‐trans‐stilbene) contribute substantially to the health benefits of this compound and are more likely to be attributable to its effect as a gene regulator.
References
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Journal ArticleDOI
Oxidative stress and diabetic complications
TL;DR: Athrosclerosis and cardiomyopathy in type 2 diabetes are caused in part by pathway-selective insulin resistance, which increases mitochondrial ROS production from free fatty acids and by inactivation of antiatherosclerosis enzymes by ROS.
Journal ArticleDOI
Nitric oxide synthases: regulation and function.
TL;DR: Nitric oxide (NO), the smallest signalling molecule known, is produced by three isoforms of NO synthase (NOS), which can be expressed in many cell types in response to lipopolysaccharide, cytokines, or other agents.
Journal ArticleDOI
Hypercholesterolemia increases endothelial superoxide anion production.
TL;DR: Increased endothelial O2- production in HV may inactivate endothelium-derived nitric oxide and provide a source for other oxygen radicals, contributing to the early atherosclerotic process.
Journal ArticleDOI
Dilated Cardiomyopathy and Neonatal Lethality in Mutant Mice Lacking Manganese Superoxide Dismutase
Yibing Li,Ting-Ting Huang,Elaine J. Carlson,Simon Melov,Philip C. Ursell,Jean L. Olson,Linda Noble,Midori P. Yoshimura,Christoph N. Berger,Christoph N. Berger,Pak H. Chan,Douglas C. Wallace,Charles J. Epstein +12 more
TL;DR: Cytochemical analysis revealed a severe reduction in succinate dehydrogenase and aconitase activities in the heart and, to a lesser extent, in other organs, which indicates that MnSOD is required for normal biological function of tissues by maintaining the integrity of mitochondrial enzymes susceptible to direct inactivation by superoxide.
Journal ArticleDOI
Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension
Ulf Landmesser,Sergey Dikalov,S. Russ Price,Louise McCann,Tohru Fukai,Steven M. Holland,William E. Mitch,David G. Harrison +7 more
TL;DR: Evidence is obtained that hypertension produces a cascade involving production of ROSs from the NADPH oxidase leading to oxidation of tetrahydrobiopterin and uncoupling of endothelial NO synthase (eNOS), which decreases NO production and increases ROS production from eNOS.
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