Evidence map›Paper›PMID 28451845›Full record

ReviewJournal of gastroenterology2017

Reflux esophagitis and its role in the pathogenesis of Barrett's metaplasia.

Rhonda Frances Souza

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

Review in Journal of gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Laryngopharyngeal Reflux Prevalence and Predictors Among Doctors.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Cellular Senescence, Inflammation, and Cancer in the Gastrointestinal Tract.International journal of molecular sciences · 2023
    Review
  13. Review
  14. Observational
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

1 author at 1 institution in 1 country.

Rhonda Frances SouzaCenter for Esophageal Research, Baylor Scott and White Research Institute, 2 Hoblitzelle, Suite 250, 3500 Gaston Avenue, Dallas, TX, 75246, USA. rhonda.souza@bswhealth.org.
Baylor Medical Center at Garland · 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
Reflux-Induced Epithelial-Mesenchymal Transition in Benign Barrett's EsophagusR01DK103598 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI SOUZA, RHONDA F, SPECHLER, STUART JON · 2015 to 2019
$1.7M
NIDDK NIH HHS R01 DK063621NIDDK NIH HHS R01 DK103598
6 · The paper itself

Abstract

Reflux esophagitis damages the squamous epithelium that normally lines the esophagus, and promotes replacement of the damaged squamous lining by the intestinal metaplasia of Barrett's esophagus, the precursor of esophageal adenocarcinoma. Therefore, to prevent the development of Barrett's metaplasia and esophageal adenocarcinoma, the pathogenesis of reflux esophagitis must be understood. We have reported that reflux esophagitis, both in a rat model and in humans, develops as a cytokine-mediated inflammatory injury (i.e., cytokine sizzle), not as a caustic chemical injury (i.e., acid burn), as traditionally has been assumed. Moreover, reflux induces activation of hypoxia inducible factor (HIF)-2α, which enhances the transcriptional activity of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) causing increases in pro-inflammatory cytokines and in migration of T lymphocytes, an underlying molecular mechanism for this cytokine-mediated injury. In some individuals, reflux esophagitis heals with Barrett's metaplasia. A number of possibilities exist for the origin of the progenitor cells that give rise to this intestinal metaplasia including those of the esophagus, the proximal stomach, or the bone marrow. However, intestinal cells are not normally found in the esophagus, the stomach, or the bone marrow. Thus, the development of Barrett's intestinal metaplasia must involve some molecular reprogramming of key developmental transcription factors within the progenitor cell, a process termed transcommitment, which may be initiated by the noxious components of the gastric refluxate. This review will highlight recent studies on the pathogenesis of reflux esophagitis and on reflux-related molecular reprogramming of esophageal squamous epithelial cells in the pathogenesis of Barrett's metaplasia.

Indexed as

AnimalsBarrett EsophagusBasic Helix-Loop-Helix ProteinsCDX2 Transcription FactorCell TransdifferentiationCellular ReprogrammingCytokinesEndothelial PAS Domain-Containing Protein 1Epithelial CellsEsophagitis, PepticHedgehog ProteinsHepatocyte Nuclear Factor 3-betaHumansNF-kappa BProto-Oncogene Proteins c-aktSignal TransductionBasic Helix-Loop-Helix ProteinsCDX2 Transcription FactorCytokinesEndothelial PAS Domain-Containing Protein 1Hedgehog ProteinsHepatocyte Nuclear Factor 3-betaNF-kappa BProto-Oncogene Proteins c-aktSOX9 Transcription FactorSOXB1 Transcription FactorsTranscription FactorsBarrett’s esophagusCdx2CytokineNF-κBSquamous cells

Identifiers

PMID28451845
PMCPMC5488728
OpenAlexW2609949613

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.