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In CVD, mitochondrial dysfunction following ischemia\u2010reperfusion (I\/R) injury results in heart failure. The proper functioning of oxidative phosphorylation (OXPHOS) and the mitochondrial life cycle in cardiac mitochondria are closely related to mitochondrial DNA (mtDNA). Following myocardial I\/R injury, mitochondria activate multiple repair and clearance mechanisms to repair damaged mtDNA. When these repair mechanisms are insufficient to restore the structure and function of mtDNA, irreversible mtDNA damage occurs, leading to mtDNA mutations. Since mtDNA mutations aggravate OXPHOS dysfunction and affect mitophagy, mtDNA mutation accumulation leads to leakage of mtDNA and proteins outside the mitochondria, inducing an innate immune response, aggravating cardiovascular injury, and leading to the need for external interventions to stop or slow the disease course. On the other hand, mtDNA released into the circulation after cardiac injury can serve as a biomarker for CVD diagnosis and prognosis. This article reviews the pathogenic basis and related research findings of mtDNA oxidative damage and mtDNA leak\u2010triggered innate immune response associated with I\/R injury in CVD and summarizes therapeutic options that target mtDNA.<\/jats:p>","DOI":"10.1155\/2022\/6235747","type":"journal-article","created":{"date-parts":[[2022,5,18]],"date-time":"2022-05-18T03:50:09Z","timestamp":1652845809000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Mitochondrial DNA Is a Vital Driving Force in Ischemia\u2010Reperfusion Injury in Cardiovascular 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