An improved understanding of mitral valve (MV) function remains an important goal for determining mechanisms underlying valve disease and for developing novel therapies. Critical to heart valve tissue homeostasis is the valvular interstitial cells (VICs), which reside in the interstitium and maintain the extracellular matrix (ECM) through both protein synthesis and enzymatic degradation [1]. There is scant experimental data on the alterations of the MV fiber network reorganization as a function of load, which is critical for implementation of computational strategies that attempt to link this meso-micro scale phenomenon. The observed large scale deformations experienced by VICs could be implicated in mechanotransduction [2], i.e., translation of mechanical stimuli into biochemical signals. Consequently, our goal is to quantitatively connect organ level loads to cellular deformation as a function of the ECM fiber network. We hypothesize that cellular deformations are likely a complex function of collagen and elastin fiber mechanical properties, architecture, and cellular coupling to these fibers.

This content is only available via PDF.
You do not currently have access to this content.