A new study from the Varelas Lab reveals that blood vessels in the lungs actively contribute to fibrotic disease progression. Led by graduate student Kostas Kontodimas, the research team used single-cell techniques and genetic tools to identify a previously unrecognized population of cells in lung veins that activate and promote tissue scarring.
Specifically, the study pinpoints defective Hippo signaling, triggered by inactivation of LATS1 and LATS2 kinases, as a key driver of vascular damage responses and pro-fibrotic signaling. Blocking downstream transcriptional activity from this disrupted pathway reduced scarring, inflammation, and blood vessel damage, opening new opportunities to develop targeted therapies for pulmonary fibrosis and related lung diseases.
Read the full publication in Science Advances
https://www.science.org/doi/10.1126/sciadv.aef8468