{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T06:13:11Z","timestamp":1788415991867,"version":"build-2803163510"},"reference-count":72,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T00:00:00Z","timestamp":1788393600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:p>Myocardial ischemia-reperfusion (I\/R) injury remains a major barrier to the full benefit of timely coronary reperfusion. This review summarizes the role of mitochondrial aldehyde dehydrogenase 2 (ALDH2) as both an endogenous cardioprotective enzyme and a potential therapeutic target in myocardial I\/R injury. During reperfusion, reactive oxygen species promote lipid peroxidation and the accumulation of cytotoxic aldehydes, particularly 4-hydroxy-2-nonenal (4-HNE) and malondialdehyde. ALDH2 detoxifies these aldehydes and thereby modulates several injury pathways, including mitochondrial dysfunction, neutrophil extracellular trap formation, ferroptosis, apoptosis, necroptosis, and maladaptive autophagy. Experimental studies consistently indicate that ALDH2 deficiency aggravates infarct size, inflammatory injury, aldehyde overload, and adverse ventricular remodeling, whereas ALDH2 activation or overexpression confers protection. Clinical and genetic studies further suggest that the ALDH2 rs671\/ALDH2*2 loss-of-function variant may influence myocardial infarction risk, reperfusion injury severity, and the response to cardioprotective strategies, especially in East Asian populations. However, the evidence remains largely preclinical, and clinical translation will require genotype-informed patient stratification, optimization of ALDH2-targeted agonists, careful timing around reperfusion, safety evaluation, and combination strategies with established reperfusion and cardioprotective approaches.<\/jats:p>","DOI":"10.3389\/fphar.2026.1846879","type":"journal-article","created":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T05:21:11Z","timestamp":1788412871000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Role of ALDH2 in myocardial ischemia-reperfusion injury: using ALDH2 as a potential therapeutic target"],"prefix":"10.3389","volume":"17","author":[{"given":"Meng","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, West China Hospital, Sichuan University","place":["Chengdu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhixiong","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fengyan","family":"Hu","sequence":"additional","affiliation":[{"name":"Wuhan Britain-China School","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, West China Hospital, Sichuan University","place":["Chengdu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,3]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"360438","DOI":"10.1155\/2014\/360438","article-title":"Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal","volume":"2014","author":"Ayala","year":"2014","journal-title":"Oxid. 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