Calcific aortic valve disease (CAVD) is a chronic process leading to fibrosis and mineralization of the aortic valve. Investigations in the last several years have emphasized that key underlying molecular processes are involved in the pathogenesis of CAVD. In this regard, the processing of lipids and their retention has been underlined as an important mechanism that triggers inflammation. In turn, inflammation promotes/enhances the mineralization of valve interstitial cells, the main cellular component of the aortic valve. On the other hand, transformation of valve interstitial cells into myofibroblasts and osteoblast-like cells is determined by several signaling pathways having reciprocal cross-talks. In addition, the mineralization of the aortic valve has been shown to rely on ectonucleotidase and purinergic signaling. In this review, the authors have highlighted key molecular underpinnings of CAVD that may have significant relevance for the development of novel pharmaceutical therapies.
Keywords: Lp-PLA2; TGF-β; Wnt; aortic stenosis; bone morphogenetic protein; calcific aortic stenosis; calcific aortic valve disease; calcification; ectonucleotidase; lipid; notch; ox-LDL.