{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T04:02:22Z","timestamp":1793160142336,"version":"4.5.0"},"reference-count":149,"publisher":"MDPI AG","issue":"5","license":[{"start":{"date-parts":[[2023,2,27]],"date-time":"2023-02-27T00:00:00Z","timestamp":1677456000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Ischemic heart disease is the principal cause of death worldwide and clinically manifests as myocardial infarction (MI), stable angina, and ischemic cardiomyopathy. Myocardial infarction is defined as an irreversible injury due to severe and prolonged myocardial ischemia inducing myocardial cell death. Revascularization is helpful in reducing loss of contractile myocardium and improving clinical outcome. Reperfusion rescues myocardium from cell death but also induces an additional injury called ischemia-reperfusion injury. Multiple mechanisms are involved in ischemia-reperfusion injury, such as oxidative stress, intracellular calcium overload, apoptosis, necroptosis, pyroptosis, and inflammation. Various members of the tumor necrosis factor family play a key role in myocardial ischemia-reperfusion injury. In this article, the role of TNF\u03b1, CD95L\/CD95, TRAIL, and the RANK\/RANKL\/OPG axis in the regulation of myocardial tissue damage is reviewed together with their potential use as a therapeutic target.<\/jats:p>","DOI":"10.3390\/ijms24054606","type":"journal-article","created":{"date-parts":[[2023,2,27]],"date-time":"2023-02-27T03:52:21Z","timestamp":1677469941000},"page":"4606","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Tumor Necrosis Factor Family Members and Myocardial Ischemia-Reperfusion Injury: State of the Art and Therapeutic Implications"],"prefix":"10.3390","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5965-6571","authenticated-orcid":false,"given":"Antonella","family":"Galeone","sequence":"first","affiliation":[{"name":"Department of Surgery, Dentistry, Pediatrics and Gynecology, Division of Cardiac Surgery, University of Verona, 37129 Verona, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7121-5899","authenticated-orcid":false,"given":"Maria","family":"Grano","sequence":"additional","affiliation":[{"name":"Department of Precision and Regenerative Medicine and Ionian Area, University of Bari Aldo Moro, 70124 Bari, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0681-1432","authenticated-orcid":false,"given":"Giacomina","family":"Brunetti","sequence":"additional","affiliation":[{"name":"Department of Biosciences, Biotechnologies and Environment, University of Bari Aldo Moro, 70125 Bari, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,2,27]]},"reference":[{"key":"ref_1","first-page":"e9349","article-title":"Global Epidemiology of Ischemic Heart Disease: Results from the Global Burden of Disease Study","volume":"12","author":"Khan","year":"2020","journal-title":"Cureus"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"H1439","DOI":"10.1152\/ajpheart.00139.2019","article-title":"Myocardial ischemia: Lack of coronary blood flow, myocardial oxygen supply-demand imbalance, or what?","volume":"316","author":"Heusch","year":"2019","journal-title":"Am. 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