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In our study, we investigated whether melatonin augments OPA1\u2010dependent mitochondrial fusion and thus maintains redox balance during myocardial I\/R injury. In hypoxia\/reoxygenation\u2010 (H\/R\u2010) treated H9C2 cardiomyocytes, melatonin treatment upregulated OPA1 mRNA and protein expression, thereby enhancing mitochondrial fusion. Melatonin also suppressed apoptosis in H\/R\u2010treated cardiomyocytes, as evidenced by increased cell viability, diminished caspase\u20103 activity, and reduced Troponin T secretion; however, silencing <jats:italic>OPA1<\/jats:italic> abolished these effects. H\/R treatment augmented mitochondrial ROS production and repressed antioxidative molecule levels, while melatonin reversed these changes in an OPA1\u2010dependent manner. Melatonin also inhibited mitochondrial permeability transition pore opening and maintained the mitochondrial membrane potential, but <jats:italic>OPA1<\/jats:italic> silencing prevented these outcomes. These results illustrate that melatonin administration alleviates cardiomyocyte I\/R injury by activating OPA1\u2010induced mitochondrial fusion and inhibiting mitochondrial oxidative stress.<\/jats:p>","DOI":"10.1155\/2022\/7105181","type":"journal-article","created":{"date-parts":[[2022,1,10]],"date-time":"2022-01-10T23:50:16Z","timestamp":1641858616000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["[Retracted] Melatonin Attenuates Ischemia\/Reperfusion\u2010Induced Oxidative Stress by Activating Mitochondrial Fusion in 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