Calcific aortic valve disease (CAVD) is one of the main causes of death from cardiovascular diseases, and its incidence and prevalence are increasing year by year. The underlying mechanism of CAVD is complex, and its pathological features are progressive fibrosis and thickening of the valve leaflets, as well as calcification of the valve, leading to left ventricular outflow tract obstruction in the late stages of the disease, which causes syncope, blackouts, and other clinical symptoms. Currently, there are no effective drugs to delay the progression of CAVD, and surgical intervention to relieve the valve stenosis is the only option. It is currently believed that the phenotypic conversion of valve interstitial cells is the cellular basis of valve calcification, and the change of the cellular microenvironment in which they are located is one of the important factors leading to phenotypic conversion. Understanding the role of cellular microenvironment changes in valve interstitial cell phenotypic conversion is helpful for us to gain a comprehensive understanding of CAVD and explore potential treatment options. In this review, we describe how the microenvironment of the valve interstitial cells affects the progression of CAVD