Evidence map›Paper›PMID 30101408›Full record

ReviewJournal of gastroenterology2019

Epithelial-stromal crosstalk and fibrosis in eosinophilic esophagitis.

Amanda B Muir, Joshua X Wang, Hiroshi Nakagawa

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. The microbiota in eosinophilic esophagitis: A systematic review.Journal of gastroenterology and hepatology · 2022
    Pooled it
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  12. Amphiregulin-producing TThe journal of allergy and clinical immunology. Global · 2024
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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

3 authors at 1 institution in 1 country.

Amanda B MuirDivision of Pediatric Gastroenterology, Hepatology, and Nutrition, The Children's Hospital of Philadelphia, Philadelphia, PA, 19104-6160, USA.
Joshua X WangDivision of Pediatric Gastroenterology, Hepatology, and Nutrition, The Children's Hospital of Philadelphia, Philadelphia, PA, 19104-6160, USA.
Hiroshi NakagawaDivision of Gastroenterology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, 956 Biomedical Research Building, 421 Curie Boulevard, Philadelphia, PA, 19104-6160, USA. nakagawh@pennmedicine.upenn.edu.
University of Pennsylvania · US

Funding

TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 1997 to 2026
$32.5M
TRAINING (CAREER DEVELOPMENT) COMPONENTU54AI117804 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI GLENN T FURUTA, Marc E. Rothenberg · 2014 to 2026
$18.5M
Autophagy and esophageal tissue remodeling in EoER01DK114436 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI NAKAGAWA, HIROSHI · 2017 to 2024
$3.1M
Lysyl oxidase mediated fibrosis in eosinophilic esophagitisK08DK106444 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI MUIR, AMANDA BROOKE · 2015 to 2019
$778k
The Role of Lysyl Oxidase in Epithelial Differentiation in Eosinophilic EsophagitisR03DK118310 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI MUIR, AMANDA BROOKE · 2019 to 2020
$264k
NIAID NIH HHS U54 AI117804NIDDK NIH HHS K08 DK106444NIDDK NIH HHS P30 DK050306NIDDK NIH HHS R01 DK114436NIDDK NIH HHS R03 DK118310
6 · The paper itself

Abstract

Eosinophilic esophagitis (EoE) is a food allergen-induced inflammatory disorder. EoE is increasingly recognized as a cause of swallowing dysfunction, food impaction and esophageal stricture. Inflammation of the esophageal mucosa involves immune cell infiltrate, reactive epithelial changes and fibroblast activation, culminating in robust tissue remodeling toward esophageal fibrosis characterized by excess collagen deposition in the subepithelial lamina propria. Fibrosis contributes to a unique mechanical property of the EoE-affected esophagus that is substantially stiffer than the normal esophagus. There is a great need to better understand the processes behind esophageal fibrosis in order to foster improved diagnostic tools and novel therapeutics for EoE-related esophageal fibrosis. In this review, we discuss the role of esophageal inflammatory microenvironment that promotes esophageal fibrosis, with specific emphasis upon cytokines-mediated functional epithelial-stromal interplays, recruitment and activation of a variety of effector cells, and tissue stiffness. We then explore the current state of clinical methodologies to detect and treat the EoE-related esophageal stricture.

Indexed as

AllergensCollagenCytokinesEosinophilic EsophagitisEsophageal MucosaFibrosisFood HypersensitivityHumansMucous MembraneAllergensCollagenCytokinesEosinophilic esophagitisFibrosisInterleukin-13MicroenvironmentTransforming growth factor-β

Identifiers

PMID30101408
PMCPMC6314980
OpenAlexW2885867066

What OpenQuestion holds

Textmetadata
LicenceTDM
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.