Importantly, studies have shown that targeting mitochondrial fission specifically at reperfusion using either mdivi-1 (a small molecule inhibitor of Drp1) [40,47] or P110 (a peptide inhibitor of the interaction between the mitochondrial fission proteins Drp1 and hFis1) [41] were also able to reduce the MI size in rodent AMI models, demonstrating the clinical applicability of this therapeutic approach. Here, DNM1L is linked to myocardial infarction.