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Lung Scarring Trigger Found in Specialized

Boston University researchers have identified a distinct population of cells in lung veins that becomes active after injury and promotes scar tissue

Boston University researchers have identified a distinct population of cells in lung veins that becomes active after...

A new study has identified a previously unknown driver of lung scarring within the body's own blood vessels. The research, published online in the journal Science Advances on August 28, 2026, was conducted by scientists from Boston University Chobanian & Avedisian School of Medicine.

Millions of people worldwide suffer from diseases that cause progressive lung scarring, known as fibrosis. This scarring severely impairs breathing and is a hallmark of conditions like pulmonary fibrosis. Treatment options remain limited and largely ineffective.

A Hidden Vascular Trigger

The collaborative study from the labs of Dr. Xaralabos Varelas and Dr. Giovanni Ligresti focused on the cells lining lung blood vessels. The team discovered a distinct population of cells located specifically in lung veins. These cells become active after injury and help create an environment that promotes scar tissue formation.

First author Kostas Kontodimas, a graduate student in the Department of Biochemistry and Cell Biology, explained the significance. "Our findings suggest that the lung's blood vessels are not simply bystanders in fibrosis but may actively drive disease through changes in the specialized cells that line the lung vasculature," he said.

The identification of this cellular driver and its associated signaling pathway offers a new opportunity for developing therapies to prevent or slow disease progression.

Tracing Scarring Cell by Cell

To understand how scarring begins, the researchers investigated whether vascular cells contribute to abnormal scar formation. They used genetically engineered experimental models and advanced laboratory techniques. A key step was selectively inactivating genes that preserve normal vascular cell function. The team then tracked how the lungs changed over time.

They analyzed thousands of individual lung cells. This allowed them to identify which cell types were affected and how they communicated during scar formation and progression. Finally, the team tested a drug that blocks the overactive signaling pathway they had identified. In preclinical models, this approach prevented lung scarring. It also reduced inflammation and blood vessel damage.

Broader Clues Beyond the Lung

The scientists believe their work challenges a traditional view of biology. Blood vessel cells are often seen as passive conduits for oxygen and nutrients. This study suggests they are active communicators.

Corresponding author Dr. Xaralabos Varelas, a professor of biochemistry and cell biology, elaborated on the wider implications. "Our findings suggest that specialized blood vessel cells actively communicate with surrounding tissues and can influence how diseases begin and progress," he said. This raises a possibility. Similar cell populations may play important roles in other diseases involving chronic inflammation or tissue scarring.

The work opens new avenues for research across a range of conditions. Additional studies are needed to determine if these findings translate to people. For now, the research provides crucial insight into how pulmonary fibrosis develops. It could ultimately lead to more effective treatments for this devastating disease.

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