Twinkle overexpression prevents cardiac rupture after myocardial infarction by alleviating impaired mitochondrial biogenesis.

The roles of mtDNA and mitochondria in the failing myocardium are well studied, but those in cardiac rupture remain unknown. Here, we demonstrated that impaired mitochondrial biogenesis accompanied by increased apoptosis and oxidative stress underlies cardiac rupture, and that mtDNA and mitochondria are potential therapeutic targets for cardiac rupture.