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Antibody and EGFR–STAT1 pathway point to new fibrosis treatments — Level B1 — a close up of a red flower

Antibody and EGFR–STAT1 pathway point to new fibrosis treatmentsCEFR B1

25 Nov 2025

Adapted from Yale, Futurity CC BY 4.0

Photo by Ian Talmacs, Unsplash

Level B1 – Intermediate
3 min
141 words

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

  • fibrosisThickening and scarring of tissue.
    fibrotic
  • monoclonalMade from identical immune cells.
  • antibodyProtein that fights infections.
  • scarringFormation of scars on tissue.
  • biomarkersIndicators of a biological condition.
  • STAT1A protein in cells that affects scarring.
  • therapiesTreatments for medical conditions.

Tip: hover, focus or tap highlighted words in the article to see quick definitions while you read or listen.

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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