EIF2A and Myocardial fibrosis: Loss of GCN2 could mitigate cardiac contractile disruption, myocardial fibrosis, apoptosis, and oxidative stress in DOX-induced cardiomyopathy by attenuating eIF2α-CHOP, and knockdown of eIF2α in the DOX-challenged H9C2 cells resulted in the higher survival rates and decreased oxidative stress 125.