Consistent results from both in vitro (retinal endothelial cells exposed to high glucose, followed by normal glucose) and in vivo (retinal microvessels from diabetic rodents maintained in poor and good glycemic control) models demonstrate the role of Drp1-mitochondrial fragmentation in the development of diabetic retinopathy and in the metabolic memory associated with its continued progression. Here, DNM1L is linked to diabetic retinopathy.