Diabetes induces cardiomyocyte apoptosis and suppresses cardiac autophagy, 
indicating that the interplay between autophagy and apoptotic cell death 
pathways is important in the pathogenesis of diabetic cardiomyopathy. The 
potential mechanism, however, remains unknown. We recently reported that 
diabetes depresses AMP-activated protein kinase (AMPK) activity, inhibits 
MAPK8/JNK1-BCL2 signaling, and promotes the interaction between BECN1 and BCL2. 
Concomitantly, diabetes induces cardiomyocyte apoptosis and suppresses cardiac 
autophagy. Activation of AMPK directly phosphorylates MAPK8, which mediates BCL2 
phosphorylation and subsequent BECN1-BCL2 dissociation, leading to restoration 
of cardiac autophagy, protection against cardiac apoptosis, and ultimately 
improvement in cardiac structure and function. We conclude that dissociation of 
BCL2 from BECN1 through activation of MAPK8-BCL2 signaling may be an important 
mechanism by which AMPK activation restores autophagy, protects against cardiac 
apoptosis, and prevents diabetic cardiomyopathy.