In the United States, Diabetic Kidney Disease (DKD) is one of the most common causes of Chronic Kidney Disease (CKD). DKD is assumed to be caused mostly by chronic hyperglycemic conditions. Clinically, however, achieving glycemic control in people with diabetes is difficult. Recent breakthroughs in mitochondrial biology have given us a new perspective on mitochondrial malfunction in DKD. A range of diabetes problems, including DKD, have been linked to reduced mitochondrial activity; moreover, aberrant mitochondrial fission may play a role in DKD development. Metformin or Sodium-Glucose coTransporter 2 (SGLT2) inhibitors have been shown to protect the kidneys by enhancing mitochondrial dynamics and lowering oxidative stress. As a result, medicines that target mitochondrial function restoration may become innovative treatment agents for DKD. Imeglimin is the first of a new family of oral anti-diabetic medications that can lower reactive oxygen species and boost mitochondrial DNA synthesis. The possible treatment strategies that impact mitochondrial activity and prevent DKD are discussed in this review
