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Moris D, Spartalis M, Tzatzaki E, et al. The role of reactive oxygen species in myocardial redox signaling and regulation. Ann Transl Med. 2017;5(16):324doi: 10.21037/atm.2017.06.17.
Moris, D., Spartalis, M., Tzatzaki, E., Spartalis, E., Karachaliou, G. S., Triantafyllis, A. S., Karaolanis, G. I., Tsilimigras, D. I., & Theocharis, S. (2017). The role of reactive oxygen species in myocardial redox signaling and regulation. Annals of translational medicine, 5(16), 324. https://doi.org/10.21037/atm.2017.06.17
Moris, Demetrios, et al. "The role of reactive oxygen species in myocardial redox signaling and regulation." Annals of translational medicine vol. 5,16 (2017): 324. doi: https://doi.org/10.21037/atm.2017.06.17
Moris D, Spartalis M, Tzatzaki E, Spartalis E, Karachaliou GS, Triantafyllis AS, Karaolanis GI, Tsilimigras DI, Theocharis S. The role of reactive oxygen species in myocardial redox signaling and regulation. Ann Transl Med. 2017 Aug;5(16):324. doi: 10.21037/atm.2017.06.17. PMID: 28861421; PMCID: PMC5566737.
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Ann Transl Med. 2017 Aug;5(16):324. doi: 10.21037/atm.2017.06.17.

The role of reactive oxygen species in myocardial redox signaling and regulation.

Annals of translational medicine

Demetrios Moris, Michael Spartalis, Eleni Tzatzaki, Eleftherios Spartalis, Georgia-Sofia Karachaliou, Andreas S Triantafyllis, Georgios I Karaolanis, Diamantis I Tsilimigras, Stamatios Theocharis

Affiliations

  1. Department of Surgery, The Ohio State University Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
  2. Division of Cardiology, Onassis Cardiac Surgery Center, Athens, Greece.
  3. Laboratory of Experimental Surgery and Surgical Research, University of Athens, Medical School, Athens, Greece.
  4. Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium.
  5. Department of Vascular Surgery, University of Athens, Medical School, Athens, Greece.
  6. Department of Pathology, Medical School, University of Athens, Athens, Greece.

PMID: 28861421 PMCID: PMC5566737 DOI: 10.21037/atm.2017.06.17

Abstract

Reactive oxygen species (ROS) are subcellular messengers in gene regulatory and signal transduction pathways. In pathological situations, ROS accumulate due to excessive production or insufficient degradation, leading to oxidative stress (OS). OS causes oxidation of DNA, membranes, cellular lipids, and proteins, impairing their normal function and leading ultimately to cell death. OS in the heart is increased in response to ischemia/reperfusion, hypertrophy, and heart failure. The concentration of ROS is determined by their rates of production and clearance by antioxidants. Increases in OS in heart failure are primarily a result of the functional uncoupling of the respiratory chain due to inactivation of complex I. However, increased ROS in the failing myocardium may also be caused by impaired antioxidant capacity, such as decreased activity of Cu/Zn superoxide dismutase (SOD) and catalase (CAT) or stimulation of enzymatic sources, including, cyclooxygenase, xanthine oxidase (XO), nitric oxide synthase, and nonphagocytic NAD(P)H oxidases (Noxs). Mitochondria are the main source of ROS during heart failure and aging. Increased production of ROS in the failing heart leads to mitochondrial permeability transition, which results in matrix swelling, outer membrane rupture, a release of apoptotic signaling molecules, and irreversible injury to the mitochondria. Alterations of "redox homeostasis" leads to major cellular consequences, and cellular survival requires an optimal regulation of the redox balance.

Keywords: Reactive oxygen species (ROS); myocardial; redox; signaling

Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

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