Article may be outdated

This article is 56 days old. Some details may have changed since publication.

Phys.org·3 min read·medium

Little-known protein helps the body restrain scar-forming signals

U
University of Manchester
Little-known protein helps the body restrain scar-forming signals
✦AI Summary

Scientists from the U.K. and U.S. have identified how a specific protein, LTBP1, regulates the TGFβ signaling molecule to prevent excessive scar tissue formation. This discovery offers new potential pathways for treating fibrosis, a condition that causes organ damage and contributes to millions of deaths annually.

Why it matters

Understanding the mechanism behind fibrosis could lead to breakthrough medical treatments for chronic organ diseases.

✦Dive DeeperCreate a free account to unlock

edited by Lisa Lock , reviewed by Robert Egan

This article has been reviewed according to Science X's editorial process and policies . Editors have highlighted the following attributes while ensuring the content's credibility:

Add as preferred source Cryo-EM structure of the LLC. Credit: Nature Communications (2026). DOI: 10.1038/s41467-026-75834-8 U.K. and U.S. scientists have uncovered an important piece of the puzzle in the signaling pathway that causes damaging scar tissue to build up in the body, raising hopes for future treatments. A team from the University of Manchester and University of Connecticut have revealed how a little-known protein helps keep one of the body's most powerful biological signals under tight control. Their findings, published in Nature Communications , could eventually help researchers develop new ways to tackle conditions linked to fibrosis, a process in which excessive scar tissue forms in organs and prevents them from working properly.

Continue reading on Headlinne

Create a free account to read the full article.

Read full article →
sciencehealth
✦

Get smarter about the news

Sign up free for a feed built around what you actually care about, Dive Deeper research on any story, and the full text of every article.

Create free account

Already have an account? Sign in