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Aortic valve calcium deposits are accumulations of calcium-containing minerals within the leaflets of the aortic valve, most commonly seen in the setting of calcific aortic valve disease (CAVD). These deposits result from an active, regulated biological process involving inflammatory infiltration, endothelial dysfunction, and the osteogenic transformation of valvular interstitial cells (VICs) into osteoblast-like cells that produce bone matrix proteins and facilitate mineralization. Calcium deposits cause stiffening and thickening ("sclerosis") of the valve, progressing to stenosis that obstructs blood flow and risks heart failure and death. Unlike most molecular targets (receptors, channels, enzymes), these deposits are a pathological product rather than a direct pharmacological target, and no currently approved drug inhibits their formation or progression, although experimental research targets pathways such as RANK/RANKL, BMP, and other regulators of osteogenesis and inflammation.
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