Inhibition of Drp1-mediated mitochondrial fission by P110 ameliorates renal injury in diabetic nephropathy.

Diabetic nephropathy (DN) is a leading cause of end-stage renal disease, characterized by progressive renal injury driven by mitochondrial dysfunction and metabolic reprogramming. Excessive mitochondrial fission, mediated by dynamin-related protein 1 (Drp1), contributes to mitochondrial fragmentation and cellular injury in the diabetic kidney. Here, we investigate the therapeutic potential of P110, a selective inhibitor of Drp1-mediated mitochondrial fission, in experimental models of DN.