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This study examined the effects of ALDH2 overexpression and knockout on diabetic cardiomyopathy and the mechanism involved with a focus on mitochondrial integrity. Mice challenged with streptozotocin (STZ, 200\u00a0mg\/kg, via intraperitoneal injection) exhibited pathological alterations, including reduced respiratory exchange ratio, dampened fractional shortening and ejection fraction, increased left ventricular end-systolic and diastolic diameters, cardiac remodeling, cardiomyocyte contractile anomalies, intracellular Ca2+ defects, myocardial ultrastructural injury, oxidative stress, apoptosis, and mitochondrial damage, which were overtly attenuated or accentuated by ALDH2 overexpression or knockout, respectively. Diabetic patients also exhibited reduced plasma ALDH2 activity, cardiac remodeling, and diastolic dysfunction. In addition, STZ challenge altered expression levels of mitochondrial proteins (PGC-1\u03b1 and UCP2) and Ca2+ regulatory proteins (SERCA, Na+\u2013Ca2+ exchanger, and phospholamban), dampened autophagy and mitophagy (LC3B ratio, TOM20, Parkin, FUNDC1, and BNIP3), disrupted phosphorylation of Akt, GSK3\u03b2, and Foxo3a, and elevated PTEN phosphorylation, most of which were reversed or worsened by ALDH2 overexpression or knockout, respectively. Furthermore, the novel ALDH2 activator torezolid, as well as the classical ALDH2 activator Alda-1, protected against STZ- or high glucose-induced in vivo or in vitro cardiac anomalies, which was nullified by inhibition of Akt, GSK3\u03b2, Parkin, or mitochondrial coupling. Our data discerned a vital role for ALDH2 in diabetic cardiomyopathy possibly through regulation of Akt and GSK3\u03b2 activation, Parkin mitophagy, and mitochondrial function.<\/jats:p>","DOI":"10.1093\/jmcb\/mjad056","type":"journal-article","created":{"date-parts":[[2023,9,27]],"date-time":"2023-09-27T20:17:09Z","timestamp":1695845829000},"source":"Crossref","is-referenced-by-count":24,"title":["Mitochondrial aldehyde dehydrogenase rescues against diabetic cardiomyopathy through GSK3<b>\u03b2<\/b>-mediated preservation of mitochondrial integrity and Parkin-mediated mitophagy"],"prefix":"10.1093","volume":"15","author":[{"given":"Yingmei","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital Fudan University , Shanghai 710032 , China"},{"name":"National Clinical Research Center for Interventional Medicine , Shanghai 200032 , 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