AKT1 and familial dilated cardiomyopathy: In STZ-induced DCM mice, cardiomyocyte cross-sectional area was increased and cardiac function was impaired; their increased phosphorylation of pro-hypertrophic signaling molecules Akt and mTOR correlated with increased phosphorylation of ERS signaling molecules GADD153, EIF2α, and IRE1α, which were ameliorated by aminoguanidine, an AGE inhibitor.