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This epidemic\u2010driven detrimental events in the cardiac tissues start with the altered distribution and metabolism pattern of high\u2010density lipoprotein\u00a0and low\u2010density lipoprotein (LDL) leading to cholesterol (oxidized LDL) deposition on the arterial wall and atherosclerotic plaque generation, followed by vascular spasms and infarction. Subsequently, obesity\u2010triggered metabolic malfunctions induce free radical generation which may further trigger pro\u2010inflammatory signaling and nuclear factor kappa\u2010light\u2010chain\u2010enhancer of activated B cells\u00a0transcriptional factor, thus inducing interferon\u2010gamma, tumor necrosis factor\u2010alpha, and inducible nitric oxide synthase. This terrifying cardiomyopathy can be further aggravated in type 2 diabetes mellitus, thereby making\u00a0obese diabetic patients prone toward\u00a0the development of myocardial infarction (MI) or stroke in comparison to their nondiabetic counterparts. The accelerated oxidative stress and pro\u2010inflammatory response induced cardiomyocyte hypertrophy, followed by apoptosis in obese diabetic individuals, causing progression of athero\u2010thrombotic vascular disease. Being an efficient antioxidative and anti\u2010inflammatory indolamine, melatonin effectively inhibits lipid peroxidation, pro\u2010inflammatory reactions, thereby resolving free radical\u2010induced myocardial damages along with maintaining antioxidant reservoir to preserve cardiovascular integrity. Prolonged melatonin treatment maintains balanced body weight and serum total cholesterol\u00a0concentration by inhibiting cholesterol synthesis and promoting cholesterol catabolism. Additionally, melatonin promotes macrophage polarization toward the anti\u2010inflammatory state, providing a proper shield during the recovery period. Therefore, the protective role of melatonin in maintaining the lipid metabolism homeostasis and blocking the atherosclerotic plaque rupture could be targeted as the possible therapeutic strategy for the management of obesity\u2010induced acute MI. This review aimed at orchestrating the efficacy of melatonin in ameliorating irrevocable oxidative cardiovascular damage induced by the obesity\u2013diabetes correlation.<\/jats:p>","DOI":"10.1111\/jpi.12847","type":"journal-article","created":{"date-parts":[[2022,12,2]],"date-time":"2022-12-02T07:33:42Z","timestamp":1669966422000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Melatonin ameliorates myocardial infarction in obese diabetic individuals: The possible involvement of macrophage apoptotic factors"],"prefix":"10.1111","volume":"74","author":[{"given":"Juin","family":"Maity","sequence":"first","affiliation":[{"name":"Oxidative Stress and Free Radical Biology Laboratory, Department of Physiology University of Calcutta Kolkata India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiyasa","family":"Dey","sequence":"additional","affiliation":[{"name":"Oxidative Stress and Free Radical 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