This review highlights the cellular and molecular alterations in the aortic valve during Calcific Aortic Valve Disease pathogenesis, emphasizing the active role of extracellular matrix components.
This review summarizes the active cellular and molecular alterations, particularly the role of the extracellular matrix, driving the pathogenesis of calcific aortic valve disease.
Calcific Aortic Valve Disease (CAVD) is the most common valvular heart disease in developed countries and in the ageing population. It is strongly correlated to median age, affecting up to 13% of the population over the age of 65. Pathophysiological analysis indicates CAVD as a result of an active and degenerative disease, starting with sclerosis and chronic inflammation and then leaflet calcification, which ultimately can account for aortic stenosis. Although CAVD has been firstly recognized as a passive event mostly resulting from a degenerative aging process, much evidences suggests that calcification arises from different active processes, involving both aortic valve-resident cells (valve endothelial cells, valve interstitial cells, mesenchymal stem cells, innate immunity cells) and circulating cells (circulating mesenchymal cells, immunity cells). Moreover, a role for the cell-derived "matrix vesicles" and extracellular matrix (ECM) components has also been recognized. The aim of this work is to review the cellular and molecular alterations occurring in aortic valve during CAVD pathogenesis, focusing on the role of ECM in the natural course of the disease.
Vito et al. (Mon,) conducted a review in Calcific Aortic Valve Disease (CAVD). This review highlights the cellular and molecular alterations in the aortic valve during Calcific Aortic Valve Disease pathogenesis, emphasizing the active role of extracellular matrix components.