SKLB023 hinders renal interstitial fibrosis in obstructive nephropathy by interfering TGF-β1/Smad3 signaling.

ABSTRACT: Renal fibrosis is the principal process underlying the progression of chronic kidney disease to end-stage renal disease. It is a relatively uniform response involving glomerulosclerosis, tubulointerstitial fibrosis and changes in renal vasculature. A considerable number of studies have confirmed that inducible nitric oxide synthase (iNOS) was highly expressed in renal interstitial fibrosis and the overexpression of iNOS played a negative role in kidney disease progression. In our previous study, SKLB023 as a novel small-molecule inhibitor of iNOS, blocked joint inflammation and cartilage destruction in arthritis. However, the pharmacological role and function of SKLB023 in renal fibrosis remained poorly understood. In the study, oral administration of SKLB023 (25 and 50 mg per kg per day)

SUBMITTER: Feng Y 

PROVIDER: S-EPMC9078199 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature