{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T04:53:09Z","timestamp":1792126389823,"version":"4.4.0"},"reference-count":129,"publisher":"Wiley","issue":"16","license":[{"start":{"date-parts":[[2025,5,31]],"date-time":"2025-05-31T00:00:00Z","timestamp":1748649600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2025,5,31]],"date-time":"2025-05-31T00:00:00Z","timestamp":1748649600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Ischaemia\u2013reperfusion injury (IRI) is a major cause of cardiomyocyte damage and death from myocardial infarction. Oxidative stress, dysregulated calcium (Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ) handling and disrupted mitochondrial dynamics are all key factors in IRI and can play a role in cell death. Mitochondria are a primary source of oxidative stress, which is generated by electron leak from the respiratory chain complexes and the oxidation of accumulated succinate upon reperfusion. The mitochondrial permeability transition pore (mPTP), a high conductance channel that forms following reperfusion of ischaemic mitochondria, has been implicated in reperfusion\u2010induced cell death. Although factors including mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    overload and oxidative stress that regulate mPTP opening have been well characterized, the composition of the mPTP is still actively investigated. Clinically, mPTP opening and IRI complicate treatment of myocardial infarction. Therefore, many possible therapeutics to reduce the damaging effects of reperfusion are under investigation. Antioxidants, pharmaceutical approaches, postconditioning and synthetic polymers have all been investigated for use in IRI. Still, many of these therapeutics of interest have shown mixed evidence underlying their use in preclinical and clinical research. In this review\u00a0we discuss our current understanding of the contributions of mitochondrial oxidative stress, mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and mitochondrial dynamics to cardiomyocyte damage and death in IRI, and where further clarification of these mechanisms is needed to identify potential therapeutic targets.\n                    <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                      <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16772-gra-0001-m.png\">\n                        <jats:alt-text>image<\/jats:alt-text>\n                      <\/jats:graphic>\n                    <\/jats:boxed-text>\n                  <\/jats:p>","DOI":"10.1113\/jp287770","type":"journal-article","created":{"date-parts":[[2025,5,31]],"date-time":"2025-05-31T13:28:47Z","timestamp":1748698127000},"page":"6659-6674","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia\u2010reperfusion injury"],"prefix":"10.1113","volume":"604","author":[{"given":"Emily","family":"Rozich","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering University of Minnesota  Minneapolis MN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9058-2168","authenticated-orcid":false,"given":"Ulas","family":"Ozkurede","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Physiology University of Minnesota  Minneapolis MN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shanmugasundaram","family":"Pakkiriswami","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Physiology University of Minnesota  Minneapolis MN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan","family":"Gemilere","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Physiology University of Minnesota  Minneapolis MN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samira M.","family":"Azarin","sequence":"additional","affiliation":[{"name":"Department of Chemical Engineering and Materials Science University of Minnesota  Minneapolis MN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8604-1633","authenticated-orcid":false,"given":"Julia C.","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Physiology University of Minnesota  Minneapolis MN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2025,5,31]]},"reference":[{"key":"e_1_2_2_2_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0708959104"},{"issue":"9","key":"e_1_2_2_3_1","first-page":"1088","article-title":"Targeting an antioxidant to mitochondria decreases cardiac ischemia\u2010reperfusion injury","volume":"19","author":"Adlam V. 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