{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T05:42:05Z","timestamp":1793770925025,"version":"4.6.1"},"reference-count":71,"publisher":"MDPI AG","issue":"16","license":[{"start":{"date-parts":[[2023,8,16]],"date-time":"2023-08-16T00:00:00Z","timestamp":1692144000000},"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>About half a century ago, Eugene Braunwald, a father of modern cardiology, shared a revolutionary belief that \u201ctime is muscle\u201d, which predetermined never-ending effort to preserve the unaffected myocardium. In connection to that, researchers are constantly trying to better comprehend the ongoing changes of the ischemic myocardium. As the latest studies show, metabolic changes after acute myocardial infarction (AMI) are inconsistent and depend on many constituents, which leads to many limitations and lack of unification. Nevertheless, one of the promising novel mechanistic approaches related to iron metabolism now plays an invaluable role in the ischemic heart research field. The heart, because of its high levels of oxygen consumption, is one of the most susceptible organs to iron-induced damage. In the past few years, a relatively new form of programmed cell death, called ferroptosis, has been gaining much attention in the context of myocardial infarction. This review will try to summarize the main novel metabolic pathways and show the pivotal limitations of the affected myocardium metabolomics.<\/jats:p>","DOI":"10.3390\/ijms241612846","type":"journal-article","created":{"date-parts":[[2023,8,16]],"date-time":"2023-08-16T09:57:02Z","timestamp":1692179822000},"page":"12846","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Cardiomyocyte Damage: Ferroptosis Relation to Ischemia-Reperfusion Injury and Future Treatment Options"],"prefix":"10.3390","volume":"24","author":[{"given":"Jolanta","family":"Laukaitiene","sequence":"first","affiliation":[{"name":"Faculty of Medicine, Medical Academy, Lithuanian University of Health Sciences, 9 A. Mickeviciaus Street, LT-44307 Kaunas, Lithuania"},{"name":"Cardiology Clinic, University Hospital, Lithuanian University of Health Sciences, Eiveniu Str. 2, LT-50161 Kaunas, Lithuania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Greta","family":"Gujyte","sequence":"additional","affiliation":[{"name":"Cardiology Clinic, University Hospital, Lithuanian University of Health Sciences, Eiveniu Str. 2, LT-50161 Kaunas, Lithuania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edmundas","family":"Kadusevicius","sequence":"additional","affiliation":[{"name":"Institute of Physiology and Pharmacology, Medical Academy, Lithuanian University of Health Sciences, 9 A. Mickeviciaus Street, LT-44307 Kaunas, Lithuania"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,8,16]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"341","DOI":"10.1136\/heartjnl-2015-307855","article-title":"Reducing myocardial infarct size: Challenges and future opportunities","volume":"102","author":"Bulluck","year":"2015","journal-title":"Heart"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"193","DOI":"10.1038\/s41420-021-00579-w","article-title":"Ferroptosis: A cell death connecting oxidative stress, inflammation and cardiovascular diseases","volume":"7","author":"Yu","year":"2021","journal-title":"Cell Death Discov."},{"key":"ref_3","doi-asserted-by":"crossref","unstructured":"Lillo-Moya, J., Rojas-Sol\u00e9, C., Mu\u00f1oz-Salamanca, D., Panieri, E., Saso, L., and Rodrigo, R. (2021). Targeting Ferroptosis against Ischemia\/Reperfusion Cardiac Injury. 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