Objective: To investigate the possible mechanism of Smurf2 in the progression of mice renal interstitial fibrosis induced by unilateral ureteral obstruction(UUO). Methods: The UUO model was established through ligating left ureters of male CD-1 mice (UUO group). At the same time,the control group were set up by sham-operation of left kidney of CD-1 male mice(sham group). The animals were sacrified at day 3,7,14 after operation. The changes of kidney structure and the lesions of renal interstitial fibrosis were observed using HE,PAS and Masson’s trichrome staining assays. Furthermore,the expressions and distributions of Smurf2,E-cadherin,alpha-smooth muscle actin (-琢-SMA) and fibronectin (FN) in obstructed and normal kidneys were detected by Western blot and immunohistochemical staining assays. Results: Compared with the sham group,at day 7 after UUO operation,the atrophy and dilution of renal tubules,renal interstitial fibrogenesis were found in the obstructed kidneys. After UUO operation,the expression of Smurf2--琢-SMA or FN protein was upregulated in an time-dependent manner,respectively;while the expression of E-cadherin was remarkably decreased. Moreover,the Smurf2 expression was mainly distributed in the nucelus of the renal tubular epithelial cells;while the distribution of -琢-SMA protein was obviously posited in renal tubular epithelial cells and renal interstitium,and the distribution of FN was in renal interstitium of the obstructed kidneys. By regression analyses,the upregulation of Smurf2 expression had positive relationship with -琢-SMA(r = 0.765,P < 0.001) and FN (r = 0.773,P < 0.01),and negative relationship with E-cadherin (r = -0.656,P < 0.001)-Conclusion: These results suggest that Smurf2 maybe act as a key in the procession of renal interstitial fibrosis of obstructive nephropathy mice through inducing renal tubular epithelial-mesenchymal transition.