Decoding the molecular drivers of lung fibrosis development and progression
Homeostatic maintenance, regeneration and repair of the lung requires precise spatiotemporal controlling and orchestrating the activities of functionally linked multilineage circuits of regenerative cell states. It is currently unknown how the dysregulation of regenerative cell states is linked to pulmonary fibrosis.
In this project, we employ single-cell multiomics and spatial profiling in fibrosing ILD patients and experimental disease models to uncover the cell-intrinsic (epigenomic) and -extrinsic (niche/microenvironmental) factors driving dysregulation of regenerative cell states and fibrosis progression, particularly focusing on immunoregulatory mechanisms.