Moreover, the present study showed that knockout of Fundc1 or specific blocking Fundc1‐mediated mitophagy by peptide with unphosphorylated Tyr18 (the active form) markedly increased cardiac infarct size and exacerbated mitochondrial and cardiac dysfunction after acute MI; and overexpression of Fundc1 dramatically ameliorated mitochondrial and cardiac functions after acute MI. Here, FUNDC1 is linked to infarction.