When inflammation in the body goes unchecked, it can cause fibrosis, or tissue scarring that may lead to organ dysfunction or even failure. This can happen in conditions such as inflammatory bowel diseases (ulcerative colitis and Crohn’s disease), chronic viral infections, interstitial lung fibrosis, chronic autoimmune skin diseases such as scleroderma, and scars associated with heart disease. Patients have few options for treating fibrosis, but new research points to a molecular pathway that could open the door to future treatment possibilities.
In earlier work, a team led by researchers at the Broad Institute and Mass General Brigham discovered a key cell type underlying fibrosis in inflammatory bowel disease (IBD). Now, in a new study in Nature, the team has characterized the crosstalk between this and other types of cells that leads to fibrosis. Their work also points to a molecule, GLIS3, that regulates this cell-to-cell communication and hadn’t been linked to IBD before. The findings suggest that interrupting this cellular pathway could one day help prevent or reduce fibrosis in patients with IBD or other diseases marked by chronic inflammation such as lung disease.





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