AIM: To investigate the relationship between autophagy and calcification in vascular smooth muscle cells( VSMCs) after plateletderived growth factor( PDGF)-BB stimulation. METHODS: Cultured VSMCs were stimulated with PDGF-BB for different time,the expression of vascular calcification-related proteins and autophagy-related proteins were detected by Western blot. The interaction between Beclin1 and PI3KC3 was detected by co-immunoprecipitation. RESULTS: The expression of BMP2 and ALP showed a trend from decline to rise. ALP slumped at 12 h,and BMP2 slumped at 6 h. Moreover,the expression of Beclin-1 showed a trend from rise to decline,and peaked at 12 h. The conversion of LC3-Ⅰto Ⅱ increased in a time-dependent manner,and peaked at 24 h. The expression of BMP2 and ALP was increased in VSMCs incubated with PDGF-BB and autophagy inhibitor 3-MA,compared with PDGFBB-stimulated VSMCs. Furthermore,the interaction between Beclin1 and PI3KC3 was enhanced at 6 h after PDGF-BB stimulated,peaked at 12 h,and kept in high level at 24 h. Moreover,the phosphorylation level of Beclin1 was enhanced by PDGF-BB stimulation,and peaked at 6 h. CONCLUSION: Our findings demonstrate that PDGF-BB-induced autophagy inhibits VSMC calcification by enhancing Beclin1 phosphorylation and interaction between Beclin1 and PI3KC3. AIM: To investigate the relationship between autophagy and calcification in vascular smooth muscle cells (VSMCs) after platelet derived growth factor (PDGF) -BB stimulation. METHODS: Cultured VSMCs were stimulated with PDGF-BB for different time, the expression of vascular calcification-related proteins and autophagy-related proteins were detected by Western blot. The interaction between Beclin1 and PI3KC3 was detected by co-immunoprecipitation. RESULTS: The expression of BMP2 and ALP showed a trend from decline to rise. ALP slumped at 12 h, and BMP2 slumped at 6 h. Moreover, the expression of Beclin-1 showed a trend from rising to decline, and peaked at 12 h. The conversion of LC3-Ito II increased in a time-dependent manner, and peaked at 24 h. The expression of BMP2 and ALP was increased in VSMCs incubated with PDGF-BB and autophagy inhibitor 3-MA, compared with PDGFBB-stimulated VSMCs. Furthermore, the interaction between Beclin1 and PI3KC3 was enhanced at 6 h after PDGF-BB stimulated, peake Moreover, the phosphorylation level of Beclin1 was enhanced by PDGF-BB stimulation, and peaked at 6 h. CONCLUSION: Our findings demonstrate that PDGF-BB-induced autophagy inhibits VSMC calcification by enhancing Beclin1 phosphorylation and interaction between Beclin1 and PI3KC3.