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During I\/R, the accumulation and oxidation of succinate contribute to reactive oxygen species (ROS) production, worsening tissue damage. Histidine triad nucleotide\u2010binding protein 3 (HINT3) is identified as a regulator of mitochondrial function and cardiomyocyte survival during I\/R. In a mouse I\/R model and an oxygen\u2010glucose deprivation\/reoxygenation (OGD\/R) model, it shows that HINT3 expression is downregulated after I\/R. Cardiomyocyte\u2010specific knockout of HINT3 exacerbates myocardial injury, impairs cardiac function, and promotes mitochondrial dysfunction and apoptosis, whereas HINT3 overexpression mitigates these effects. Mechanistically, HINT3 interacts with succinate dehydrogenase subunit A (SDHA), suppresses HDAC1 expression, and prevents SDHA deacetylation at K335, reducing SDH activity and mitochondrial ROS production. These findings highlight the HINT3\u2010HDAC1\u2010SDHA axis as a key pathway in mitochondrial regulation, offering new insights and therapeutic targets for myocardial reperfusion injury.<\/jats:p>","DOI":"10.1002\/advs.202503109","type":"journal-article","created":{"date-parts":[[2025,8,4]],"date-time":"2025-08-04T09:09:36Z","timestamp":1754298576000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["The Role of HINT3 in Myocardial Ischemia\u2010Reperfusion Injury in Male Mice: Mechanisms Involving SDHA and its Acetylation"],"prefix":"10.1002","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9077-1949","authenticated-orcid":false,"given":"Jiabin","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University  Wuhan 430060 P. R. China"},{"name":"Hubei Key Laboratory of Metabolic and Chronic Diseases  Wuhan 430060 P. R. 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