Aim: Epithelial-mesenchymal transition (EMT) is a process by which injured renal tubular epithelial cell undergo a phenotypic conversion into mesenchymal cell and an important pathway to generation fibroblast in renal fibrosis. Autophagy is a cellular process of degradation of damaged cytoplasmic components and regulates cell death or proliferation. It is unclear whether autophagy plays a role in TGF-β induced tubular EMT. In this study, we investigated the role of autophagyin TGF-β induced tubular EMT and renal fibrosis induced by UUO by using conditional knockout mice in which autophagy gene 7 (Atg7) is genetically ablated specifically in tubular epithelial cell. Methods: Atg7-floxed mice were crossed with Ksp-Cre mice to generate tubular-epithelial cell-specific Atg7 knockout mice (Atg7flox/flox;Ksp-Cre+). Unilateral ureteral obstruction (UUO) was performed and mice were sacrificed 3, 7 and 14 days after UUO. Results: In vitro, TGF-β treatment in HK2 cell induced autophagy in dose-dependent and time-dependent manner. In vivo, after UUO, tubular cell apoptosis and renal fibrosis were markedly more induced in Atg7flox/flox;Ksp-Cre+ than in wild-type mice. The expression of TGF-β was more increased in Atg7flox/flox;Ksp-Cre+ than in wild-type mice. The expression of E-cadherin was more decreased and the expression of α-smooth muscle antibody and vimentin were more increased in Atg7flox/flox;Ksp-Cre+ than in wild-type mice. Conclusions: Our data demonstrate that autophagy regulates apoptosis of tubular epithelial cells and renal fibrosis through TGF-β induced EMT.