Fibrotic diseases cause excessive scar tissue and can be life‑threatening. Yale researchers report two related findings that point to new treatments. In Blood they describe a human monoclonal antibody that targets epiregulin, a signaling molecule that binds EGFR. Earlier work had found higher epiregulin in skin from patients with scleroderma.
The team compared single-cell RNA sequencing from scleroderma and fibrotic graft‑versus‑host disease and confirmed upregulated epiregulin as a shared feature. They tested the antibody in humanized mouse models and in patient skin biopsies and found that inhibiting epiregulin reduced biomarkers associated with fibrosis.
In Nature Communications they show greater STAT1 activity in fibroblasts from fibrotic diseases. Mouse and cell experiments confirmed that STAT1 is required for fibrotic gene activation, and EGFR can activate STAT1 independently of JAKs. The researchers plan further tests in lupus and hidradenitis suppurativa.
Difficult words
- fibrosis — Thickening and scarring of tissue.fibrotic
- monoclonal — Made from identical immune cells.
- antibody — Protein that fights infections.
- scarring — Formation of scars on tissue.
- biomarkers — Indicators of a biological condition.
- STAT1 — A protein in cells that affects scarring.
- therapies — Treatments for medical conditions.
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Discussion questions
- What do you think about new treatments for fibrotic diseases?
- How can research in this area benefit patients?
- Why is it important to understand the role of epiregulin?
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