MAPK3 and diabetic cardiomyopathy: Similarly, glucose, AGE, and methylglyoxal, the precursor of AGE, could enhance apoptosis of human cardiac myocytes and collagen deposition, an important event of diabetic cardiomyopathy, in rat cardiac fibroblasts accompanied by temporal activation of ERK1/2, p38 MAPK, and nuclear O-GlcAcylation [13,29,30].