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Reactive oxygen and nitrogen species (ROS\/RNS) modify\u00a0cellular structures and functions by means of covalent changes in proteins including among others\n                    <jats:italic>S<\/jats:italic>\n                    \u2010nitros(yl)ation by nitric oxide (NO) and its derivatives, and\n                    <jats:italic>S<\/jats:italic>\n                    \u2010sulphydration by hydrogen sulphide (H\n                    <jats:sub>2<\/jats:sub>\n                    S). Many enzymes are involved in the mitochondrial formation and handling of ROS, NO and H\n                    <jats:sub>2<\/jats:sub>\n                    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\n                    <jats:sub>2<\/jats:sub>\n                    S play also a role in endogenous cardioprotection, as in the case of ischaemic pre\u2010conditioning, so that preventing their increase might hamper self\u2010defence mechanisms. The aim of the present review was to provide a critical analysis of formation and role of reactive species, NO and H\n                    <jats:sub>2<\/jats:sub>\n                    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\n                    <jats:sub>2<\/jats:sub>\n                    S is likely to reveal novel molecular targets for cardioprotection that could be modulated by pharmacological agents to prevent I\/R injury.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.15279","type":"journal-article","created":{"date-parts":[[2020,5,8]],"date-time":"2020-05-08T05:46:34Z","timestamp":1588916794000},"page":"6510-6522","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":88,"title":["The role of mitochondrial reactive oxygen species, NO and H\n                    <sub>2<\/sub>\n                    S in ischaemia\/reperfusion injury and cardioprotection"],"prefix":"10.1111","volume":"24","author":[{"given":"Ioanna","family":"Andreadou","sequence":"first","affiliation":[{"name":"Laboratory of Pharmacology Faculty of Pharmacy National and Kapodistrian University of Athens Athens 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