Abstract
The aim of the present study was to examine the regulatory mechanism underlying the depression in Ski‑related novel protein N (SnoN) in diabetic nephrology (DN). NRK‑52E cells, a rat primary renal tubular epithelial cell line, were cultured to clarify the effect of small mothers against decapentaplegic (Smad) ubiquitination regulatory factor 2 (smurf2) on SnoN in a low glucose environment in vitro. NRK‑52E cells and DM rats were injected with adenoviruses AD‑smurf2 and AD‑shsmurf2, respectively, and the protein expression profiles of SnoN, smurf2 and phosphorylated (p)‑Smad2 were then detected. In addition, the protein levels of smurf2, p‑Smad2 and SnoN were analyzed following treatment with transforming growth factor (TGF)‑β1 or TGF‑β1 inhibitor to validate the effect of the TGF‑β1/Smad signaling pathway. The effect of smurf2 on the degradation of SnoN by ubiquitination was found to be a key factor in DN, which was mediated by the TGF‑β1/Smad signaling pathway.