Venous lung cells drive fibrosis in preclinical models

A lung injury does not switch every blood-vessel cell into the same response. In experimental models, researchers at Boston University Chobanian & Avedisian School of Medicine found that a distinct population of cells in lung veins becomes active after injury and helps build the environment in which scar tissue forms.

The team, led by Dr. Xaralabos Varelas and Dr. Giovanni Ligresti, used genetically engineered models and laboratory techniques to selectively inactivate genes that preserve normal vascular-cell function. They then tracked the lungs over time and analyzed thousands of individual lung cells to see which populations changed and how they communicated during scarring. The work, published in Science Advances, links LATS1/2 inactivation to this venous endothelial response.

The researchers also tested a drug that blocks the overactive signaling pathway. In preclinical models, blocking that signal prevented lung scarring while reducing inflammation and blood-vessel damage. The result does not yet constitute a treatment for patients: the measurements came from experimental models, and further studies are needed to establish whether the same cell population and pathway drive fibrosis in people.

The concrete implication is a new place to look for therapies for pulmonary fibrosis and other diseases involving chronic inflammation or tissue scarring. Instead of treating blood vessels as passive conduits for oxygen and nutrients, the study suggests that specialized vascular cells can communicate with nearby tissue and influence disease progression. For patients, that could eventually mean an additional strategy to slow lung damage; for now, the advance remains at the laboratory stage.