Mitochondria from Fundc1 KO mouse hearts after acute MI showed significantly decreased Δψm and increased ROS production compared with mitochondria from either Beclin1+/− hearts or wild‐type hearts after acute MI (Figure 4B,C), suggesting that Fundc1 deficiency caused mitochondrial impairment exacerbates mitochondrial dysfunction after acute MI. This evidence concerns the gene FUNDC1 and myocardial infarction.