During myocardial ischemia/reperfusion injury, the increased expression and activation of DRP1 can cause increased mitochondrial fission and disruption of mitochondrial homeostasis, leading to cell apoptosis and loss of cardiac function.17,38 Our study also revealed that DDX17/BCL6-DRP1 is a novel regulatory pathway of mitochondrial homeostasis and cardiac function with important functions in maintaining cardiomyocyte function under physiological conditions and inhibiting the development of heart failure under pathological conditions (Fig. 6g). This evidence concerns the gene DNM1L and heart failure.