Heart valve calcification is a condition where calcium buildup in the valve causes tissue stiffening, narrowed valve opening, reduced flow output, and even failure of the valve. Calcification results from either fibroblastic or osteogenic differentiation of valvular interstitial cells (VICs) and involves a complex biochemical process that responds to the mechanical stresses and strains experienced by the valve tissue. Therefore, there is a strong interplay of the fluid-structure interaction (FSI) of the valve and the biochemical formation of calcification. Here we present a multiscale and Multiphysics framework that integrates 3D FSI of the aortic valve with a systems biology model of calcification chemical kinetics to simulate calcification progression over time. The FSI simulations will be solved using an in-house immersed boundary code and will capture the mechanical strains in the tissue and the wall shear stresses from the flow. The system biology model will utilize the stress and strain data and solve the chemical kinetics equations governing signaling pathways such as Nitric Oxide (NO) synthesis, LDL cholesterol penetration, TGF-beta/SMAD signaling, and their effects on calcium uptake into the leaflet tissue. We conduct FSI simulations of three aortic valve configurations with varying thicknesses from 0.3 to 0.75 mm, corresponding to different degrees of fibrosis. Our results reveal a strong link between valvular fibrosis and the effective lifespan of the valve. A more fibrotic valve exhibits impaired opening kinetics, leading to lower wall shear stress, reduced endothelial NO synthesis, and increased LDL penetration. These factors collectively accelerate calcification, suggesting that fibrosis-driven mechanical changes are key contributors to early valve failure. In the future, this Multiphysics framework could potentially be used as patient-specific models predicting the long-term progression of heart valve calcification and also as a computational framework to study therapeutic intervention of calcification.