Mechanisms of Lung Fibrosis
Lung fibroblasts stained for F-actin fibers (red) and transcriptional co-activator YAP (green)
Despite recent approval of two new therapies, many patients with idiopathic pulmonary fibrosis (IPF) continue to have progressive disease, impaired exercise capacity, and poor quality of life. Clearly more effective and targeted therapy for IPF could have a positive impact on the well-being of the numerous people affected by this disease.
The Medoff lab studies multiple aspects in the pathogenesis of pulmonary fibrosis. This includes the role of YAP-TAZ signaling in pulmonary fibroblast activation, the role of ROCK1 and ROCK2 in driving IPF, as well as translational studies looking to discover novel inhibitors of IPF. These studies include large screens to identify inhibitors of fibroblast activation and cell-specific delivery of ROCK inhibitors. More recently the lab has been working to characterize the transcriptional landscape in the lung in IPF and studying mechanisms of fibrosis after severe respiratory virus infections such as influenza and SARS-CoV2.