C-reactive protein promotes diabetic kidney disease via Smad3-mediated NLRP3 inflammasome activation.

ABSTRACT: Diabetic kidney disease (DKD) is the leading cause of end-stage kidney diseases resulting in enormous socio-economic burden. Accumulated evidence has indicated that C-reactive protein (CRP) exacerbates DKD by enhancing renal inflammation and fibrosis through TGF-β/Smad3 signaling. NLRP3 inflammasome is the key sensor contributing to renal inflammation. However, whether CRP enhances inflammation in DKD via NLRP3 inflammasome-related pathway remains unknown. In this study, we demonstrate that CRP promotes DKD via Smad3-mediated NLRP3 inflammasome activation as mice overexpressing human CRP gene exhibits accelerated renal inflammation in diabetic kidneys, which is associated with the activation of Smad3 and NLRP3 inflammasomes. In contrast, blockade of CPR signaling with a neutralizing anti-C

SUBMITTER: Wang Y 

PROVIDER: S-EPMC11764780 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature