| Literature DB >> 23978413 |
Juliane C Campos1, Kátia M S Gomes, Julio C B Ferreira.
Abstract
Reactive oxygen and nitrogen species regulate a wide array of signaling pathways that governs cardiovascular physiology. However, oxidant stress resulting from disrupted redox signaling has an adverse impact on the pathogenesis and progression of cardiovascular diseases. In this review, we address how redox signaling and oxidant stress affect the pathophysiology of cardiovascular diseases such as ischemia-reperfusion injury, hypertension and heart failure. We also summarize the benefits of exercise training in tackling the hyperactivation of cellular oxidases and mitochondrial dysfunction seen in cardiovascular diseases.Entities:
Keywords: ()OH; 4-HNE; 4-hydroxy-2-nonenal; ATP; Bioenergetics; Cardiac disease; Cu ZnSOD; ETC; Free radicals; GPX; GSH; GSSG; H(2)O(2); HNO; MAO; MDA; MnSOD; NADH; NADPH oxidase isoform; NAPDH; NO(); NO(+); NOS; NOX; ONOO(); Oxidative metabolism; Oxidative stress; Physical activity; RNS; ROS; SOD; VO(2) max; adenosine triphosphate; constitutive endothelial NOS; copper–zinc superoxide dismutase; eNOS; electron transport chain; glutathione peroxidase; hydrogen peroxide; hydroxyl radical; iNOS; inducible NOS; malondialdehyde; manganese superoxide dismutase; maximal oxygen consumption; mitochondrial nitric oxide synthase; monoamine oxidase; mtNOS; nicotinamide adenine dinucleotide; nicotinamide adenine dinucleotide phosphate; nitric oxide; nitric oxide synthase; nitrogen dioxide; nitrosonium; nitroxyl; oxidized glutathione; peroxynitrite; reactive nitrogen species; reactive oxygen species; reduced glutathione; superoxide; superoxide dismutase
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Year: 2013 PMID： 23978413 DOI： 10.1016/j.fct.2013.08.035
Source DB: PubMed Journal: Food Chem Toxicol ISSN： 0278-6915 Impact factor: 6.023