Calcific aortic valve disease: The role of the stem cell niche

Abstract

Calcific Aortic Valve Disease is the most common indication for surgical valve replacement in the world [1]. For years this disease was thought to be a passive degenerative phenomenon. Understanding of the cellular mechanisms of this valve lesion will provide new cellular therapeutic options to slow disease progression. Until recently the etiology of valvular heart disease has been thought to be a degenerative process related to the passive accumulation of calcium binding to the surface of the valve leaflet. Recent descriptive studies have demonstrated the critical features of aortic valve calcification, including osteoblast expression, cell proliferation and atherosclerosis [2-5] and mitral valve degeneration, glycosaminglycan accumulation, proteoglycan expression, and abnormal collagen expression [6-9]. Studies have demonstrated that specific bone cell phenotypes are present in calcifying valve specimens in human specimens [10, 11]. This phenotype is the foundation for the studies focused on the cellular mechanism for osteoblastogenesis in the heart and the foundation for the Molecular Biology of Valvular Disease.