High-glucose-induced cardiomyocyte injury is the major cause of diabetic 
cardiomyopathy, but its regulatory mechanisms are not fully understood. Here, we 
report that a circadian clock gene, brain and muscle Arnt-like 1 (Bmal1), 
increases autophagy in high-glucose-induced cardiomyocyte injury. We constructed 
a hyperglycemia model with cultured cardiomyocytes from neonatal rats. 
High-glucose-induced inhibition of autophagy and cardiomyocyte injury were 
attenuated by Bmal1 overexpression and aggravated by its knockdown. Furthermore, 
autophagy stabilization by 3-methyladenine or rapamycin partially suppressed the 
effects of altered Bmal1 expression on cardiomyocyte survival. Mechanistically, 
Bmal1 mediated resistance to high-glucose-induced inhibition of autophagy at 
least partly by inhibiting mTOR signaling activity. Collectively, our findings 
suggest that the clock gene Bmal1 is a positive regulator of autophagy through 
the mTOR signaling pathway and protects cardiomyocytes against high-glucose 
toxicity.