Abstract
Calcific aortic valve disease (CAVD) is the most common degenerative heart valve disease. Among the many risk factors for this disease are age, hypercholesterolemia, hypertension, smoking, type-2 diabetes, rheumatic fever, and chronic kidney disease. Since many of these overlap with risk factors for atherosclerosis, the molecular and cellular mechanisms of CAVD development have been presumed to be similar to those for atherogenesis. Thus, attempts have been made to evaluate the therapeutic efficacy of statins, representative anti-atherosclerosis drugs with lipid-lowering and anti-inflammatory effects, against CAVD. Unfortunately, statins have shown little or no effect on CAVD development. But some reports suggest that statins may prevent or reduce the development of early stage CAVD in which having calcification is absent or minimal. These results suggest that therapeutic approaches should differ according to the stage of disease, and that a precise understanding of the mechanism of aortic valve calcification is required to identify novel therapeutic targets for advanced CAVD. Given the involvement of inflammatory processes in the development and progression of CAVD, current therapeutic approaches for chronic inflammatory cardiovascular disease like atherosclerosis may help to prevent or minimize the early development of CAVD. In this review, we focus on several inflammatory cellular and molecular components involved in CAVD that might be considered drug targets for preventing CAVD.