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However, the regulatory mechanisms underlying cardiomyocyte oxidative stress during myocardial infarction are not fully understood. In the present study, we explored the cardioprotective action of optic atrophy 1\u2010 (Opa1\u2010) mediated mitochondrial autophagy (mitophagy) in oxidative stress\u2010challenged cardiomyocytes, with a focus on mitochondrial homeostasis and the MAPK\/ERK pathway. Our results demonstrated that overexpression of Opa1 in cultured rat H9C2 cardiomyocytes, a procedure that stimulates mitophagy, attenuates oxidative stress and increases cellular antioxidant capacity. Activation of Opa1\u2010mediated mitophagy suppressed cardiomyocyte apoptosis by downregulating Bax, caspase\u20109, and caspase\u201012 and upregulating Bcl\u20102 and c\u2010IAP. Using mitochondrial tracker staining and a reactive oxygen species indicator, our assays showed that Opa1\u2010mediated mitophagy attenuated mitochondrial fission and reduced ROS production in cardiomyocytes. In addition, we found that inhibition of the MAPK\/ERK pathway abolished the antioxidant action of Opa1\u2010mediated mitophagy in these cells. Taken together, our data demonstrate that Opa1\u2010mediated mitophagy protects cardiomyocytes against oxidative stress damage through inhibition of mitochondrial fission and activation of MAPK\/ERK signaling. These findings reveal a critical role for Opa1 in the modulation of cardiomyocyte redox balance and suggest a potential target for the treatment of myocardial infarction.<\/jats:p>","DOI":"10.1155\/2021\/3726885","type":"journal-article","created":{"date-parts":[[2021,6,8]],"date-time":"2021-06-08T19:45:30Z","timestamp":1623181530000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Protective Effect of Optic Atrophy 1 on Cardiomyocyte Oxidative Stress: Roles of Mitophagy, Mitochondrial Fission, and MAPK\/ERK 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