Objective: To investigate the calcification mechanism of bicuspid aortic valve(BAV) which involves the microRNA-195. Methods: Stenotic BAV or degenerative tricuspid aortic valve(DTV) samples were collected from 35 patients undergoing aortic valve replacement. The mRNA expression of miRNA-195 and SMAD7, and protein expression of SMAD7 were determined by RT-PCR and Western blot, respectively. Dual-luciferase assay was performed to determine putative target of miRNA-195. In porcine valve interstitial cells(VIC) ,we down-regulated and up-regulated the microRNA-195 level, and examine the mRNA expression of SMAD7 to explore the relationship between miRNA-195 and SMAD7. Moreover, in human leaflet samples, immunochemistry staining was carried out to test the protein expression of MMP-2 and MMP-9, and Sirus Red staining was done to investigate the expression of collagen, and the Von Kossa staining was implemented to explore the mineralization nodes. All of these were done to compare the functional alteration associated with cellular calcification. Results: Compared with TAV, the expression of miRNA-195 was remarkably lower in BAV with higher expression of SMAD7. Luciferase experiments validated that miRNA-195 directly targeted SMAD7. Overexpression of miRNA-195 inhibited the mRNA expression of SMAD7, while miRNA-195 inhibitor treatment resulted in increased SMAD7 expression in VIC. Finally, more MMP-2 and MMP-9 expression and more collagen distribution were observed in BAV than in DTV. Conclusion: Our study has demonstrated that miRNA-195 is much more down-regulated in stenotic BAV than that in DTV. The downregulation of miRNA-195 promotes valvular calcification via targeting SMAD7, which involves the fibrosis of extracellular matrix.