Cell and ECM Mechanotransduction in Wound Healing and Fibrosis, ECM-based biomaterials for Tissue Regeneration, Molecular Evolution, Cooperative Materials Systems
My lab is primarily focused on both understanding and manipulating cell-ECM mechanotransduction pathways in homeostasis and disease. Our primary interest is in understanding how cells' changing microenvironment direct their phenotype and initiate pathological programs, primarily tissue fibrosis and scar formation. Both cells and their extracellular matrix (ECM) are exquisitely sensitive to mechanical forces and slight perturbations in the mechanical homeostasis between cells and their ECM can initiate pathological programs that lead to tissue destruction and even death. For example, pulmonary fibrosis is a fatal disease driven in large part by stiffening of lung tissue due to chronic wound repair. Once the tissue becomes stiff, normal cells are recruited into a pathological program that ultimately leads to complete destruction of the lung and death of the patient. There are no cures and very few viable medical options for treating the disease. For these reasons, understanding how the fibrotic program is both initiated and persists will lead to new breakthroughs in treating these fatal diseases.