Evidence map›Paper›PMID 23019192›Full record

ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2012

Tissue remodeling in eosinophilic esophagitis.

Edaire Cheng, Rhonda F Souza, Stuart J Spechler

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
11.5field-weighted citation impact, top 1% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

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  18. Amphiregulin-producing TThe journal of allergy and clinical immunology. Global · 2024
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14 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Edaire ChengDepartments of Pediatrics, Children’s Medical Center, USA.
Rhonda F Souza
Stuart J Spechler
Children's Medical Center · USVA North Texas Health Care System · US

Funding

Role of Acid in the Development of Barrett's EsophagusR01DK063621 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI SOUZA, RHONDA F, SPECHLER, STUART JON · 2002 to 2015
$3.4M
ANTECEDANTS SEQUELAE OF CHILDHOOD ONSET DISEASEK12HD068369 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI SKAPEK, STEPHEN X · 2011 to 2020
$3.0M
Basic and Clinical Studies on the Role of Bile Acids in Barrett's EsophagusR01CA134571 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI SOUZA, RHONDA F, SPECHLER, STUART JON · 2009 to 2013
$1.3M
NCI NIH HHS R01-CA134571NICHD NIH HHS K12 HD068369NICHD NIH HHS K12HD-068369-01NIDDK NIH HHS R01 DK063621NIDDK NIH HHS R01-DK63621
6 · The paper itself

Abstract

Eosinophilic esophagitis (EoE) is a recently recognized, immune-mediated disease characterized clinically by symptoms of esophageal dysfunction and histologically by eosinophil-predominant inflammation. The chronic esophageal eosinophilia of EoE is associated with tissue remodeling that includes epithelial hyperplasia, subepithelial fibrosis, and hypertrophy of esophageal smooth muscle. This remodeling causes the esophageal rings and strictures that frequently complicate EoE and underlies the mucosal fragility that predisposes to painful mucosal tears in the EoE esophagus. The pathogenesis of tissue remodeling in EoE is not completely understood, but emerging studies suggest that secretory products of eosinophils and mast cells, as well as cytokines produced by other inflammatory cells, epithelial cells, and stromal cells in the esophagus, all contribute to the process. Interleukin (IL)-4 and IL-13, Th2 cytokines overproduced in allergic disorders, have direct profibrotic and remodeling effects in EoE. The EoE esophagus exhibits increased expression of transforming growth factor (TGF)-β1, which is a potent activator of fibroblasts and a strong inducer of epithelial-mesenchymal transition. In addition, IL-4, IL-13, and TGF-β all have a role in regulating periostin, an extracellular matrix protein that might influence remodeling by acting as a ligand for integrins, by its effects on eosinophils or by activating fibrogenic genes in the esophagus. Presently, few treatments have been shown to affect the tissue remodeling that causes EoE complications. This report reviews the potential roles of fibroblasts, eosinophils, mast cells, and profibrotic cytokines in esophageal remodeling in EoE and identifies potential targets for future therapies that might prevent EoE complications.

Indexed as

Cell Adhesion MoleculesEosinophilic EsophagitisEosinophilsEpithelial-Mesenchymal TransitionHumansInterleukin-13Interleukin-4Mast CellsTh2 CellsTransforming Growth Factor betaCell Adhesion MoleculesInterleukin-13Interleukin-4POSTN protein, humanTransforming Growth Factor beta

Identifiers

PMID23019192
PMCPMC3532456
OpenAlexW2108703504

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.