Τίτλος:
The role of mitochondrial reactive oxygen species, NO and H2S in ischaemia/reperfusion injury and cardioprotection
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
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 (H2S). Many enzymes are involved in the mitochondrial formation and handling of ROS, NO and H2S 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 H2S 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 H2S 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 H2S is likely to reveal novel molecular targets for cardioprotection that could be modulated by pharmacological agents to prevent I/R injury. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
Συγγραφείς:
Andreadou, I.
Schulz, R.
Papapetropoulos, A.
Turan, B.
Ytrehus, K.
Ferdinandy, P.
Daiber, A.
Di Lisa, F.
Περιοδικό:
Journal of Cellular and Molecular Medicine
Εκδότης:
Blackwell Publishing Inc.
Λέξεις-κλειδιά:
cryopyrin; cyclic GMP dependent protein kinase; cyclophilin D; cytochrome b; cytochrome c; cytochrome c oxidase; glutathione; hydrogen sulfide; inducible nitric oxide synthase; inflammasome; isocitrate dehydrogenase; myoglobin; nicotinamide adenine dinucleotide phosphate; nitric oxide; nitric oxide synthase; oxoglutarate dehydrogenase; reactive oxygen metabolite; succinate dehydrogenase; transcription factor Nrf2; xanthine oxidase; cardiotonic agent; hydrogen sulfide; nitric oxide; reactive oxygen metabolite, cardiomyopathy; catalysis; energy metabolism; energy resource; enzyme activity; heart injury; heart protection; human; mitochondrial biogenesis; mitochondrial permeability; mitochondrial respiration; mitochondrion; oxidation; oxidative stress; priority journal; reperfusion injury; respiratory chain; Review; signal transduction; animal; heart mitochondrion; metabolism; myocardial ischemia reperfusion injury, Animals; Cardiotonic Agents; Humans; Hydrogen Sulfide; Mitochondria, Heart; Myocardial Reperfusion Injury; Nitric Oxide; Reactive Oxygen Species
