ACSL4 and familial dilated cardiomyopathy: In this study, we found for the first time that MARK4 expression was increased in the STZ-induced model and that reducing MARK4 expression in the myocardia of DCM mice inhibited oxidative stress and myocardial apoptosis, promoted mitochondrial fusion and ACSL4-mediated lipid oxidative metabolism, and played a cardioprotective role (Fig. 9).