Motivation
Soft tissue has a remarkable ability to adapt to changes in mechanical loading. For example, it has been observed that the aorta tends to thicken in response to elevated blood pressure to reduce the increased load of the vessel wall. While this adaptation can be directly observed on the tissue scale, the mediators are the tissue-resident cells. In this project, we focused on developing a computational model that includes cellular signal processing to address the multiscale nature of mechanobiology.
Methods
We model cellular signal processing as a coupled system of ordinary differential equations and capture long-range biochemical interactions between cells via diffusion-reaction equations. The mechanical behavior of soft tissue is described using standard nonlinear continuum mechanics. The multiscale model is implemented in a finite element code based on several open-source libraries.
Results
The model can successfully reproduce previously observed experimental and computational results. In addition, it allows us to study how genetic defects (on the molecular/protein level) might translate to maladaptive tissue responses (on the tissue level) and how different cell types communicate to maintain tissue form and function.