Evidence map›Paper›PMID 41068129›Full record

ArticleNature communications2025

EGFR-STAT1 pathway drives fibrosis initiation in fibroinflammatory skin diseases.

Anahi V Odell, Nathan M Newton, Anna Eisenstein, Goran Micevic, Richard A Flavell, Ian D Odell

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Trial
  2. Discovery of a novel and potent KRASJournal of enzyme inhibition and medicinal chemistry · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Anahi V OdellDepartment of Dermatology, Yale University School of Medicine, New Haven, CT, USA.
Nathan M NewtonDepartment of Dermatology, Yale University School of Medicine, New Haven, CT, USA.
Anna EisensteinDepartment of Dermatology, Yale University School of Medicine, New Haven, CT, USA.
Goran MicevicDepartment of Dermatology, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0003-0329-1053
Richard A FlavellDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA. Richard.flavell@yale.edu.ORCID http://orcid.org/0000-0003-4461-0778
Ian D OdellDepartment of Dermatology, Yale University School of Medicine, New Haven, CT, USA. ian.odell@yale.edu.ORCID http://orcid.org/0000-0003-3990-6929

Funding

INTERDISCIPLINARY IMMUNOLOGY TRAINING PROGRAMT32AI007019 · NIAID · YALE UNIVERSITY · PI Carrie L. Lucas, David G. Schatz · 1985 to 2026
$14.4M
Epidermal Growth Factor Receptor Signaling in Fibrotic Skin DiseaseK08AR077689 · NIAMS · YALE UNIVERSITY · PI ODELL, IAN D · 2021 to 2025
$861k
Interrogation of T cell Bystander Activation in SclerodermaR03AR083454 · NIAMS · YALE UNIVERSITY · PI ODELL, IAN D · 2024 to 2024
$147k
NIAID NIH HHS T32 AI007019NIAMS NIH HHS K08 AR077689NIAMS NIH HHS R03 AR083454
6 · The paper itself

Abstract

Chronic inflammatory skin diseases affect the health of millions of people worldwide, and those that feature fibrosis are refractory to treatments. The signals that determine whether fibrosis occurs during chronic skin inflammation are poorly understood. We generated a scRNA-seq atlas of seven inflammatory skin diseases and their healthy controls. Diseases with fibrosis demonstrate higher expression and activity of STAT1 in fibroblasts. Fibroblast STAT1 is required for skin fibrosis development in mice. STAT1 activation promotes a fibrotic gene expression profile which can be activated directly by EGFR in a JAK-independent manner and abrogated by genetic and pharmacologic STAT1 inhibition. The EGFR-STAT1 pathway is stimulated by high affinity EGFR ligands expressed by activated keratinocytes, suggesting keratinocyte-derived signals as triggers of skin fibrosis. In sum, fibroinflammatory skin diseases are characterized by fibroblast EGFR-STAT1 signaling that controls expression of fibrotic genes, elucidating an interferon independent function of STAT1 to mediate fibrotic skin diseases.

Indexed as

ErbB ReceptorsSkin DiseasesSTAT1 Transcription FactorAnimalsFemaleFibroblastsFibrosisHumansInflammationKeratinocytesMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionSkinEGFR protein, humanEGFR protein, mouseErbB ReceptorsSTAT1 protein, humanStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID41068129
PMCPMC12511620

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.