Aortic Valve (AV) calcification is a degenerative disease that results in AV sclerosis and is one of the major causes of death. AV is subjected to mechanical conditions such as fluid shear stress, transvalvular pressure and membrane tension1. Normal hemodynamic conditions constantly renew and remodel the valve, whereas altered mechanical loading has been implicated to be the cause of AV disease2. Studies have shown that adverse hemodynamics such as hypertension and altered shear stress can cause tissue inflammation that leads to calcification and stenosis3, 4, and ultimately result in valve failure. However, the molecular and cellular processes that lead to calcification are not very well understood.

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