Aim To observe the effect of angiotensinⅡ (AngⅡ) on the autophagy of mouse aortic smooth muscle cells and the regulation of autophagy on cell phenotype conversion. Methods Mouse vascular smooth muscle cells were obtained by primary culture, vascular smooth muscle cells were incubated with 10－6 mol/L AngⅡ at different time, Western blot was used to detect the expression of LC3-Ⅱ. Transmission electron microscope was used to observe the autophagic body of different groups. Vascular smooth muscle cells were pretreated with 3-MA, Baf-A1 and then incubated with 10－6 mol/L AngⅡ for 24 h, Western blot was used to detect the expression of LC3-Ⅱ and the contractile phenotype marker (SM22α and SM-α-actin) and synthetic phenotype marker (OPN) of vascular smooth muscle cells in different groups. qRT-PCR was performed to detect the Atg7 mRNA level after transfection with siRNA Atg7. Western blot was performed to detect the expression of LC3-Ⅱ, SM22α, SM-α-actin and OPN to observe the effect of siRNA Atg7 on AngⅡ-induced autophagy and VSMC phenotype conversion. Results AngⅡ stimulated LC3-Ⅱ expression in a time-dependent manner, 3-MA significantly attenuated the AngⅡ-enforced expression of LC3-Ⅱ while Baf-A1 further increased the expression of LC3-Ⅱ. Both 3-MA and Baf-A1 significantly suppressed AngⅡ-stimulated VSMC phenotype conversion. Transfection with siRNA Atg7 remarkably decreased the expression of LC3-Ⅱ stimulated by AngⅡ and suppressed AngⅡ-stimulated VSMC phenotype conversion. Conclusion AngⅡ-stimulated VSMC phenotype conversion may be autophagy-dependent, and inhibition of autophagy significantly suppressed AngⅡ-stimulated VSMC phenotype conversion.