In addition, using mdivi-1 to inhibit Drp1 can increase the proportion of extended mitochondria in cardiomyocytes, delay the opening of mitochondrial permeability transition pore (mPTP), reduce acute IRI-induced cell death, and reduce the area of myocardial infarction caused by IRI, indicating that the inhibition of Drp1 has potential therapeutic effect. Here, DNM1L is linked to myocardial infarction.