The role of mitochondrial reactive oxygen species, NO and H2S in ischaemia/reperfusion injury and cardioprotection. Issue 12 (8th May 2020)

• Record Type: Journal Article
• Authors: Andreadou, Ioanna; Schulz, Rainer; Papapetropoulos, Andreas; Turan, Belma; Ytrehus, Kirsti; Ferdinandy, Peter; Daiber, Andreas; Di Lisa, Fabio
• Is Part Of: Journal of cellular and molecular medicine. Volume 24:Issue 12(2020)
• Page Start: 6510
• Page End: 6522
• Publication Date: 2020-05-08
• Subjects: cardioprotection -- heart -- hydrogen sulphide -- ischaemia -- mitochondria -- nitric oxide -- reactive oxygen species -- reperfusion; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.15279
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Redox signalling in mitochondria plays an important role in myocardial ischaemia/reperfusion (I/R) injury and in cardioprotection. Reactive oxygen and nitrogen species (ROS/RNS) modify cellular structures and functions by means of covalent changes in proteins including among others S ‐nitros(yl)ation by nitric oxide (NO) and its derivatives, and S ‐sulphydration by hydrogen sulphide (H2 S). Many enzymes are involved in the mitochondrial formation and handling of ROS, NO and H2 S under physiological and pathological conditions. In particular, the balance between formation and removal of reactive species is impaired during I/R favouring their accumulation. Therefore, various interventions aimed at decreasing mitochondrial ROS accumulation have been developed and have shown cardioprotective effects in experimental settings. However, ROS, NO and H2 S play also a role in endogenous cardioprotection, as in the case of ischaemic pre‐conditioning, so that preventing their increase might hamper self‐defence mechanisms. The aim of the present review was to provide a critical analysis of formation and role of reactive species, NO and H2 S in mitochondria, with a special emphasis on mechanisms of injury and protection that determine the fate of hearts subjected to I/R. The elucidation of the signalling pathways of ROS, NO and H2 S is likely to reveal novel molecular targets for cardioprotection that could be modulated by pharmacological agents to prevent I/R injury.