The hallmarks of advanced calcific aortic valve stenosis include massive accumulation of amorphous or bone-like calcium and the excessive production and accrual of collagen and extracellular matrix proteins. These histopathological changes are frequently associated with increases in valvular lipid deposition, inflammatory cell infiltrate, pro-inflammatory cytokine elaboration, and matrix metalloproteinase expression. In the search for key mechanisms underlying the calcification and fibrosis that drive progression of valvular stenosis, animal models have played an integral role. To date, mouse models of hypercholesterolemia have been the predominant model of choice [1-4].
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