Dr. Kharanan Sharma
Oakland University, Rochester, MI
Abstract
Mechanotransduction is the mechanism by which mechanical forces cause the heart to remodel. Researchers understand qualitatively that mechanotransduction can arise from the coupling of the cytoskeleton and extracellular matrix by integrins in the cell membrane. A complete description of mechanotransduction, however, requires this idea be expressed quantitatively using a mathematical model. To be useful, this model must predict where mechanotransduction occurs in the heart. Predicting growth and remodeling in response to mechanotransduction could be useful for understanding cardiac disease, and could be relevant to tissue engineering. The mechanical bidomain model is a multiscale mathematical model that represents cardiac tissue as a continuum yet accounts for forces across the myocardial membrane. The model's central hypothesis is that membrane forces acting on integrins are responsible for mechanotransduction, and that these forces arise from differences between intracellular and extracellular displacements. The model predicts different regions of mechanotransduction and remodeling than does the traditional monodomain model.
