The role of mitochondrial reactive oxygen species, NO and H2S in ischaemia/reperfusion injury and cardioprotection

Ioanna Andreadou, Rainer Schulz, Andreas Papapetropoulos, Belma Turan, Kirsti Ytrehus, Peter Ferdinandy, Andreas Daiber, Fabio Di Lisa

Research output: Contribution to journalReview articlepeer-review

5 Scopus citations

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 (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.

Original languageEnglish (US)
Pages (from-to)6510-6522
Number of pages13
JournalJournal of Cellular and Molecular Medicine
Volume24
Issue number12
DOIs
StatePublished - Jun 1 2020

Keywords

  • cardioprotection
  • heart
  • hydrogen sulphide
  • ischaemia
  • mitochondria
  • nitric oxide
  • reactive oxygen species
  • reperfusion

ASJC Scopus subject areas

  • Molecular Medicine
  • Cell Biology

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