Research Areas

Our research defines epithelial mechanisms of lung injury and repair in fibrotic lung disease. We focus on how syndecan-1 regulates alveolar type 2 (AT2) cell dysfunction and senescence, promoting aberrant repair and persistent fibrosis to identify targets that restore normal lung repair.

We investigate how syndecan-1 regulates alveolar type 2 (AT2) cell fate and function. Our work defines how syndecan-1-mediated signaling disrupts epithelial homeostasis, leading to impaired repair and fibrotic remodeling.

We study how cellular senescence in AT2 cells contributes to maladaptive, dysplastic repair. These processes drive persistent fibrosis and limit the lung’s regenerative capacity.

Leveraging a clinical biorepository, we integrate human lung tissues and longitudinal clinical data to study epithelial dysfunction and validate mechanisms in fibrotic lung disease and other conditions.