MFN2 and diabetic retinopathy: The same in vivo model has shown suboptimal mitochondrial levels of Mfn2 and continued development of retinal histopathology and characteristic of diabetic retinopathy, even after removal of hyperglycemic insult [23], suggesting that the retinal vasculature experiences both downregulated fusion process and upregulated fission process, and mitochondria continue to be fragmented, further confirming the role of mitochondrial dynamics in the metabolic memory phenomenon.