Furthermore, inhibition of Fis1 or Drp1 expression prevents high-glucose-induced ROS generation and mitochondrial fragmentation in venous endothelial cells with elevated levels of Fis1 protein in patients with atherosclerosis and increased abundance of Fis1 and Drp1 proteins in human aortic endothelial cells cultured in high-glucose medium (Mai et al., 2010). This evidence concerns the gene DNM1L and atherosclerosis.