Background and aim of the study: Calcific aortic valve disease (CAVD) is a commonly acquired valvular disease. Although previous studies have shown valve calcification to be mediated by a chronic inflammatory disease process, with many similarities to atherosclerosis that included inflammatory cell infiltrates, lipoproteins, lipids, extracellular bone-matrix proteins, and bone minerals, little is known of the mechanisms of the cellular and molecular components and processes. It has recently been hypothesized that the calcific aortic valve is a product of active inflammation, similar to the atherosclerosis pathological process. Thus, the cessation of statin therapy should, in theory, have an effect on the treatment of CAVD and on aortic valve myofibroblasts (AVMFs), which play an important role in aortic valvular calcification. The study aim was to determine if oxidized low-density lipoprotein (oxLDL) could stimulate the apoptosis of AVMFs and the calcific-related pathway, and whether atorvastatin could inhibit the effects of AVMFs induced by oxLDL. The Wnt/GSK-3 beta/beta-catenin signaling pathway may play a key role in this process, thereby making a major contribution to aortic valve calcification. Methods: AVMFs were successfully acquired using a combination of trypsin and collagenase enzyme digestion, and made phenotypic for the identification for alpha-smooth muscle actin (alpha-SMA). Cell apoptosis was monitored using flow cytometry, bone protein expression by Western blot, and related gene expression by reverse transcription polymerase chain reaction (RT-PCR). Results: A positive identification of alpha-SMA, a myofibroblast marker, confirmed the successful harvesting of myofibroblasts. OxLDL significantly induced cell apoptosis (p <0.05), and this became even more obvious after 48 h (p <0.01). OxLDL also significantly increased the protein expression of all differentiation markers (p <0.05), as confirmed through Western blotting and RT-PCR, while atorvastatin significantly reduced the effects of oxLDL (p <0.05). Conclusion: Among the mechanisms of the cellular and molecular components and processes, oxLDL increased the valve calcification-related signaling pathway by increasing extracellular bone-matrix protein that produces osteoblastic gene markers via the Wnt/GSK-3 beta/beta-catenin pathway. And atorvastatin also prevented any oxLDL-induced effects through the same pathway, this may represent a new therapeutic target for CAVD, as an alternative to traditional valve replacement surgery.