At the organelle level, mitochondrial mass is maintained by mitochondrial synthesis, fusion and fission, and removal of damaged mitochondria.36 In experiments with pressure overload-induced myocardial hypertrophy and heart failure mouse model, the results showed that the increased autophagy in response to pressure overload occurs concurrently with DRP1 mitochondrial translocation, and upregulation of DRP1 aggravates pressure overload induction of cardiac dysfunction.37 Excessive mitochondrial fission is mainly caused by the upregulation or activation of DRP1. Here, DNM1L is linked to heart failure.