Evidence map›Paper›PMID 27842700›Full record

ArticleThe American journal of pathology2016

The Aryl Hydrocarbon Receptor and Its Ligands Inhibit Myofibroblast Formation and Activation: Implications for Thyroid Eye Disease.

Collynn F Woeller, Elisa Roztocil, Christine L Hammond, Steven E Feldon, Richard P Phipps

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
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

28 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Targeting the Aryl Hydrocarbon Receptor to Attenuate IGF1R Signaling in Thyroid Eye Disease.Thyroid : official journal of the American Thyroid Association · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. AhR and Wnt/β-Catenin Signaling Pathways and Their Interplay.Current issues in molecular biology · 2023
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
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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

5 authors at 1 institution in 1 country.

Collynn F WoellerDepartment of Environmental Medicine, School of Medicine and Dentistry, University of Rochester, Rochester, New York.
Elisa RoztocilFlaum Eye Institute, School of Medicine and Dentistry, University of Rochester, Rochester, New York.
Christine L HammondFlaum Eye Institute, School of Medicine and Dentistry, University of Rochester, Rochester, New York.
Steven E FeldonFlaum Eye Institute, School of Medicine and Dentistry, University of Rochester, Rochester, New York.
Richard P PhippsDepartment of Environmental Medicine, School of Medicine and Dentistry, University of Rochester, Rochester, New York; Flaum Eye Institute, School of Medicine and Dentistry, University of Rochester, Rochester, New York. Electronic address: richard_phipps@urmc.rochester.edu.
University of Rochester · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Martha Susiarjo · 1985 to 2026
$42.8M
Aryl Hydrocarbon Receptor Ligands and Thyroid Eye DiseaseR01EY023239 · NEI · UNIVERSITY OF ROCHESTER · PI PHIPPS, RICHARD P. · 2013 to 2016
$1.4M
Thy1 expression, adpogenesis, inflammation and orbital remodeling mechanisms in Thyroid Eye DiseaseR01EY027308 · NEI · UNIVERSITY OF ROCHESTER · PI FELDON, STEVEN E · 2017 to 2019
$1.2M
Environmental obesogens reduce Thy1 expression and promote obesityR21ES023032 · NIEHS · UNIVERSITY OF ROCHESTER · PI PHIPPS, RICHARD P. · 2013 to 2014
$420k
NEI NIH HHS R01 EY023239NEI NIH HHS R01 EY027308NIEHS NIH HHS P30 ES001247NIEHS NIH HHS R21 ES023032
6 · The paper itself

Abstract

Thyroid eye disease (TED) is a degenerative disease that manifests with detrimental tissue remodeling, myofibroblast accumulation, and scarring in the orbit of affected individuals. Currently, there are no effective therapies for TED that target or prevent the excessive tissue remodeling caused by myofibroblast formation and activation. The canonical cytokine that induces myofibroblast formation is transforming growth factor (TGF)-β. The TGF-β signaling pathway is influenced by aryl hydrocarbon receptor (AHR) signaling pathways. We hypothesized that AHR agonists can prevent myofibroblast formation in fibroblasts from patients with TED, and thus AHR ligands are potential therapeutics for the disease. Orbital fibroblasts explanted from patients with TED were treated with TGF-β to induce myofibroblast formation, contraction, and proliferation. We found that AHR ligands prevent TGF-β-dependent myofibroblast formation, and this ability is dependent on AHR expression. The AHR and AHR ligands block profibrotic Wnt signaling by inhibiting the phosphorylation of GSK3β to prevent myofibroblast formation. These results provide new insight into the molecular pathways underlying orbital scarring in TED. These novel studies highlight the potential of the AHR and AHR ligands as future therapeutic options for eye diseases and possibly also for other scarring conditions.

Indexed as

Wnt Signaling PathwayCells, CulturedFibroblastsGene Knockdown TechniquesGraves DiseaseHumansLigandsMyofibroblastsOrbital DiseasesReceptors, Aryl HydrocarbonRNA, Small InterferingThyroid GlandTransforming Growth Factor betaLigandsReceptors, Aryl HydrocarbonRNA, Small InterferingTransforming Growth Factor beta

Identifiers

PMID27842700
PMCPMC5225292
OpenAlexW2556035065

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.