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Calcific Aortic Valve Disease (CAVD) occurs in >2% of the population over 65 years of age and often leads to valvular stenosis that necessitates valve replacement [1]. CAVD is a pro‐ gressive disease, often manifesting first as aortic valve sclerosis and later developing into stenosis and valve dysfunction [2]. The specific molecular and cellular mechanisms of CAVD initiation and advancement are not well defined, and inhibitors of CAVD progres‐ sion have not been identified. The current standard of treatment for CAVD is aortic valve replacement [3]. Presently, there are no pharmacologic-based treatments for CAVD, and new therapeutic approaches for CAVD are needed. The majority of aortic valves that are re‐ placed have congenital malformations, such as bicuspid aortic valve (BAV), establishing a link between valve development and disease mechanisms [4].

Developmental Pathways in CAVD