The role of extracellular matrix dysregulation in fibrotic lung disease
My previous work has helped define actin cytoskeleton-associated proteins that sense ECM-related forces and convert these physical cues into biochemical signals affecting cell fate and function. Although ECM dysregulation is a hallmark of fibrotic lung diseases (e.g. idiopathic pulmonary fibrosis and asthma), precisely how cells sense and respond to pathological ECM remains poorly understood. My group now employs a combination of biophysical, bioengineering, and biochemical approaches to unravel the role of ECM dysregulation in lung diseases. Ultimately, greater understanding of the crosstalk between cells and ECM in the context of fibrosis will reveal the best strategies to target mechanically regulated signaling pathways for therapeutic benefit.