Molecular and cellular mechanisms of valve calcification

Abstract

Aortic valve stenosis is the most common form of acquired valvular disease, with a prevalence of 1% to 2% in people over the age of 65 years. Untreated, the presence of severe symptoms is associated with a life expectancy of less than 5 years. Relatively little is known about the role of the cells within the valve or the regulatory pathways that are involved in the onset and progression of the disease. The aim of this article is to review the role played by valve interstitial and endothelial cells and highlight the role of pathways and individual mediators that have been implicated in playing a role in the disease process. This includes mediators that regulate pro- and anti-calcification mechanisms. The clinical significance of calcium within the valve is discussed, as are the therapeutic opportunities that may allow for development of a medical therapy for aortic stenosis. Understanding the molecular and cellular mechanism of valve calcification will allow development of alternative therapies to surgical replacement of the valve and improve prognosis of patients with aortic stenosis.