The role of reactive oxygen species in the pathophysiology of cardiovascular diseases and the clinical significance of myocardial redox

Acute and chronic excessive intracellular increase of reactive oxygen species (ROS) is involved in the development and progression of cardiovascular diseases. ROS are by-products of various oxidative physiological and biochemical processes. Sources of ROS are mitochondrial respiration, NADH/NADPH ox...

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Bibliographic Details
Published in:Annals of translational medicine Vol. 5; no. 16; p. 326
Main Authors: Moris, Demetrios, Spartalis, Michael, Spartalis, Eleftherios, Karachaliou, Georgia-Sofia, Karaolanis, Georgios I, Tsourouflis, Gerasimos, Tsilimigras, Diamantis I, Tzatzaki, Eleni, Theocharis, Stamatios
Format: Journal Article
Language:English
Published: China AME Publishing Company 01-08-2017
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Summary:Acute and chronic excessive intracellular increase of reactive oxygen species (ROS) is involved in the development and progression of cardiovascular diseases. ROS are by-products of various oxidative physiological and biochemical processes. Sources of ROS are mitochondrial respiration, NADH/NADPH oxidase, xanthine oxidoreductase or the uncoupling of nitric oxide synthase (NOS) in vascular cells. ROS mediate various signaling pathways that underlie cardiovascular pathophysiology. The delicate equilibrium between free-radical generation and antioxidant defense is altered in favor of the former, thus leading to redox imbalance, oxidative stress, and increased cellular injury. An understanding of the pathophysiological mechanisms mediated by oxidative stress is crucial to the prevention and treatment of cardiovascular diseases.
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Contributions: (I) Conception and design: D Moris; (II) Administrative support: E Spartalis, S Theocharis; (III) Provision of study materials or patients: GI Karaolanis, DI Tsilimigras; (IV) Collection and assembly of data: M Spartalis, E Tzatzaki, G Tsourouflis; (V) Data analysis and interpretation: D Moris, M Spartalis, GS Karachaliou; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.
ISSN:2305-5839
2305-5839
DOI:10.21037/atm.2017.06.27