The DRP1-FLNa interaction leads to mitochondrial hyperfission, which is associated with myocardial senescence and heart failure after myocardial infarction (MI), whereas inhibition of the DRP1-FLNa complex formation can suppress hypoxia-mediated mitochondrial fragmentation and attenuate the progression of heart failure after MI (Nishimura et al., 2018). This evidence concerns the gene DNM1L and myocardial infarction.