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


Journal Article (Review)

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.

Full Text

Duke Authors

Cited Authors

  • Moris, D; Spartalis, M; Spartalis, E; Karachaliou, G-S; Karaolanis, GI; Tsourouflis, G; Tsilimigras, DI; Tzatzaki, E; Theocharis, S

Published Date

  • August 2017

Published In

Volume / Issue

  • 5 / 16

Start / End Page

  • 326 -

PubMed ID

  • 28861423

Pubmed Central ID

  • 28861423

Electronic International Standard Serial Number (EISSN)

  • 2305-5847

International Standard Serial Number (ISSN)

  • 2305-5839

Digital Object Identifier (DOI)

  • 10.21037/atm.2017.06.27


  • eng