Asprosin Aggravates Tubular Epithelial Cell Injury and Phenotypic Transformation via Mitochondrial Dynamics Disorder Mediated by Excessive Drp1 SUMOylation in Diabetic Nephropathy Mice.

ABSTRACT: Epidemiological studies show that some diabetic patients develop end-stage renal dysfunction without significant proteinuria or glomerulopathy, underscoring the role of renal tubular epithelial cell (TEC) impairment in diabetic kidney disease (DKD). However, the primary pathogenic determinants underlying TEC impairment and disease advancement in DKD progression remain unclear. This study reveals that asprosin (ASP) is up-regulated and positively correlated with kidney dysfunction in DKD mice. Moreover, elevated ASP is mainly located in the renal TEC, and negatively impacts TEC. In addition, supraphysiological ASP concentration impairs mitochondrial dynamics and function in both DKD mice and HK2 cells. Mechanistically, ASP promotes Drp1 over-SUMOylation, thus reducing Drp1 degradation and d

SUBMITTER: Huang Q 

PROVIDER: S-EPMC12533405 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature