Deubiquitinating enzymes as therapeutic targets in diabetic nephropathy

Diabetic nephropathy (DN), a leading cause of chronic kidney disease and end-stage renal disease, remains a major clinical challenge. Current therapeutic strategies primarily delay rather than prevent disease progression, highlighting the urgent need for novel interventions. Emerging evidence implicates deubiquitinating enzymes (DUBs) in the dysregulation of key pathological processes in DN, including glycolipid metabolism, oxidative stress, inflammation, and fibrosis. By modulating the stability and activity of critical substrates, DUBs exert context-dependent dual roles in DN pathogenesis. This review summarizes current insights into the regulatory roles of DUBs in DN pathogenesis and discusses their potential as promising therapeutic targets for future clinical intervention.