Atherosclerosis and aortic stenosis are two of the most prevalent cardiovascular disorders and a major cause of death in elderly population. In atherosclerosis, plaques and calcium deposits build up inside major arteries, which lead to narrowing of the vessel lumens and limits or completely blocks blood flow. Similarly, in calcific aortic stenosis, calcium deposits on valve cusps and valve ring result in narrowing of valve lumen, eventually leading to impaired function and even valve failure. As the disease progresses, both diseases thus require expensive replacement/repair surgeries in most patients. However, in spite of the high prevalence, the causes and mechanisms of these diseases are still not clearly understood. Due to the similarities in diseased tissue pathology, atherosclerosis and aortic stenosis have been suggested to be continuum of the same disease [1] and mainly have been investigated for atherosclerosis. However, the prevalence of both diseases is not concurrent in most patients. Likewise, valvular interstitial cells (VICs) were thought to behave in a similar manner as smooth muscle cells (SMCs), but some recent studies suggest differences between the two cell types [2]. Therefore, unique mechanisms might be involved in how VICs and SMCs respond to an osteogenic environment.

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