Open AccessThe role of mitochondrial reactive oxygen species, NO and H 2 S in ischaemia/reperfusion injury and cardioprotection
Author(s) -
Andreadou Ioanna,
Schulz Rainer,
Papapetropoulos Andreas,
Turan Belma,
Ytrehus Kirsti,
Ferdinandy Peter,
Daiber Andreas,
Di Lisa Fabio
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15279
Subject(s) - cardioprotection , reactive oxygen species , mitochondrion , reactive nitrogen species , reperfusion injury , nitric oxide , chemistry , ischemia , microbiology and biotechnology , mitochondrial ros , pharmacology , biochemistry , biology , medicine , organic chemistry
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 (H 2 S). Many enzymes are involved in the mitochondrial formation and handling of ROS, NO and H 2 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 H 2 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 H 2 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 H 2 S is likely to reveal novel molecular targets for cardioprotection that could be modulated by pharmacological agents to prevent I/R injury.