Objective: To evaluate the effects of Ang II on epithelial-mesenchymal transition (EMT) in podocytes and to explore whether homocysteine (Hcy) could aggravate it and the possible mechanisms. Design and method: A recently generated conditionally immortalized mouse podocyte cell line was cultivated as described before. Podocytes were divided into three groups, control group (CG), Ang II group (AG) and Hcy + Ang II group (H + A G). Podocytes of AG and H + A G were exposed to Ang II (10–6 mol/l) for 24 h, and meanwhile podocytes of H + A G were exposed to Hcy (8∗10–4 mol/l) for 24 h. All cells were FBS-deprived for 12 h before each experiment. EMT is characterized by loss of nephrin and observation of mesenchymal marker such as desmin. The expression of nephrin and desmin were assessed by quantitative real-time PCR (qRT-PCR) and Western blotting. The expression of AKT and p-AKT were assessed by Western blotting. Results: (1) Compared with CG, nephrin mRNA and protein were obviously decreased and desmin mRNA and protein were increased significantly (P < 0.05) in AG. (2) The decrease in nephrin and the increase in desmin were much more significant in H + A G than those in AG (P < 0.05). (3) An increased expression of P-AKT/AKT was observed in podocytes in H + A G, when compared with that in AG (P < 0.05). Conclusions: Ang II is a contributing factor to EMT in podocytes and Hcy could aggravate Ang II induced EMT via PI3K / AKT signaling pathway.