Evidence map›Paper›PMID 31536596›Full record

ArticlePloS one2019

Proton pump inhibitors attenuate myofibroblast formation associated with thyroid eye disease through the aryl hydrocarbon receptor.

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

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Targeting the Aryl Hydrocarbon Receptor to Attenuate IGF1R Signaling in Thyroid Eye Disease.Thyroid : official journal of the American Thyroid Association · 2025
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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.

Christine L HammondFlaum Eye Institute, School of Medicine and Dentistry, University of Rochester, Rochester, New York, United States of America.
Elisa RoztocilFlaum Eye Institute, School of Medicine and Dentistry, University of Rochester, Rochester, New York, United States of America.
Richard P PhippsDepartment of Environmental Medicine, School of Medicine and Dentistry, University of Rochester, Rochester, New York, United States of America.
Steven E FeldonFlaum Eye Institute, School of Medicine and Dentistry, University of Rochester, Rochester, New York, United States of America.
Collynn F WoellerFlaum Eye Institute, School of Medicine and Dentistry, University of Rochester, Rochester, New York, United States of America.ORCID 0000-0001-7197-5057
University of Rochester · US

Funding

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
NEI NIH HHS R01 EY023239NEI NIH HHS R01 EY027308
6 · The paper itself

Abstract

Thyroid eye disease (TED) can lead to scar formation and tissue remodeling in the orbital space. In severe cases, the scarring process leads to sight-threatening pathophysiology. There is no known effective way to prevent scar formation in TED patients, or to reverse scarring once it occurs. In this study, we show that the proton pump inhibitors (PPIs), esomeprazole and lansoprazole, can prevent transforming growth factor beta (TGFβ)-mediated differentiation of TED orbital fibroblasts to myofibroblasts, a critical step in scar formation. Both PPIs prevent TGFβ-induced increases in alpha-smooth muscle actin (αSMA), calponin, and collagen production and reduce TED orbital fibroblast cell proliferation and migration. Esomeprazole and lansoprazole exert these effects through an aryl hydrocarbon receptor (AHR)-dependent pathway that includes reducing β-catenin/Wnt signaling. We conclude that PPIs are potentially useful therapies for preventing or treating TED by reducing the myofibroblast accumulation that occurs in the disease.

Indexed as

ActinsCalcium-Binding ProteinsCalponinsCell DifferentiationCells, CulturedCicatrixCollagenEsomeprazoleFibroblastsGraves OphthalmopathyHEK293 CellsHumansLansoprazoleMicrofilament ProteinsMyofibroblastsProton Pump InhibitorsACTA2 protein, humanActinsCalcium-Binding ProteinsCalponinsCollagenEsomeprazoleLansoprazoleMicrofilament ProteinsProton Pump InhibitorsReceptors, Aryl HydrocarbonTransforming Growth Factor beta

Identifiers

PMID31536596
PMCPMC6752849
OpenAlexW2974618842

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.