In addition, high glucose levels promote the expression of mitochondrial fission-related proteins, such as dynamin-related protein 1 (Drp1) and fission 1 (Fis1), thereby impairing mitochondrial function, promoting ROS accumulation, reducing eNOS activity and NO bioavailability, and aggravating endothelial dysfunction (57, 58). Here, DNM1L is linked to endothelial dysfunction.