Fig. 8From: Grpel2 maintains cardiomyocyte survival in diabetic cardiomyopathy through DLST-mediated mitochondrial dysfunction: a proof-of-concept studySchematic illustration of a novel molecular mechanism. Schematic illustration of a novel molecular mechanism by which the reduction of Nr2f6-regulated Grpel2 expression results in mitochondrial dysfunction in diabetic heart. Nr2f6 binds to the Grpel2 promoter to promote the Grpel2 expression. Diabetes-induced Nr2f6 reduction decreased the Grpe2 expression, which inhibited the import process of DLST into mitochondria. Afterward, the deficiency of DLST in mitochondria results in mitochondrial dysfunction, including increased ROS content, decreased ATP contents and decreased mitochondrial membrane potential, eventually aggravating DCMBack to article page