  This article reviews the mechanical bidomain model, a mathematical
description how the extracellular matrix and intracellular cytoskeleton are
coupled by integrin proteins. The fundamental hypothesis is that differences
between intracellular and extracellular displacements drive
mechanotransduction. A one-dimensional example illustrates the model, which is
then extended to two dimensions. In several cases the equations are solved
analytically, illustrating how displacements divide into two parts: monodomain
displacements are identical in both spaces and therefore do not contribute to
mechanotransduction, whereas bidomain displacements cause mechanotransduction.
A new length constant depends on the intracellular and extracellular shear
moduli and the integrin spring constant, and bidomain effects often occur
within a few length constants of the tissue edge. Numerical methods for solving
the model equations are being developed. Precursors to the model and potential
applications are discussed. The bidomain model may be applicable to cardiac
remodeling, blood vessel regulation, tissue engineering, stem cell
differentiation, cancer biology, and development.
