Take home figure.

GRK4 aggravates cardiac ischemic injury via inhibiting autophagy in a HDAC4-dependent way. Autophagy activity is protective for cardiomyocyte apoptosis in post-myocardial infarction heart. Nuclear accumulated HDAC4 regulates the binding of FoxO3a with beclin1 promoter, thereby increasing the expression of beclin1 and autophagy. Ischaemic injury stimulates GRK4 expression in cardiomyocyte. Elevated GRK4 translocate into nuclei, phosphorylates HDAC4 and promotes its nuclear export. This inhibits the effect of HDAC4 on autophagy, thereby aggravating cardiomyocyte apoptosis and cardiac remodeling.