Evidence map›Paper›PMID 35672395›Full record

ReviewNature reviews. Gastroenterology & hepatology2022

Mechanisms and pathophysiology of Barrett oesophagus.

Rhonda F Souza, Stuart J Spechler

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Advances in the Diagnosis of Barrett's Esophagus.Diagnostics (Basel, Switzerland) · 2026
    Review
  6. Article
  7. Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026
    Review
  8. Article
  9. Recent advances in spasmolytic polypeptide expressing metaplasia research.World journal of gastrointestinal oncology · 2026
    Review
  10. Article
  11. Article
  12. Pathogenesis of Barrett's Esophagus: Evolving and Emerging Mechanisms.Gastrointestinal endoscopy clinics of North America · 2026
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Reflux Esophagitis.The Korean journal of helicobacter and upper gastrointestinal research · 2025
    Review
  20. Article
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

2 authors at 1 institution in 1 country.

Rhonda F SouzaDivision of Gastroenterology, Center for Oesophageal Diseases, Baylor University Medical Center, Dallas, TX, USA. Rhonda.Souza@BSWHealth.org.ORCID http://orcid.org/0000-0003-3484-2807
Stuart J SpechlerDivision of Gastroenterology, Center for Oesophageal Diseases, Baylor University Medical Center, Dallas, TX, USA.
Baylor University Medical Center · US

Funding

The Role of APE1/Ref-1 in Reflux-Induced Epithelial-Mesenchymal Transition in Benign Barrett's Metaplasia: A Novel Target for Preventing Recurrent Barrett's Esophagus After Radiofrequency AblationR01DK124185 · NIDDK · BAYLOR RESEARCH INSTITUTE · PI SOUZA, RHONDA F, SPECHLER, STUART JON · 2020 to 2023
$1.4M
NIDDK NIH HHS R01 DK124185
6 · The paper itself

Abstract

Barrett oesophagus, in which a metaplastic columnar mucosa that can predispose individuals to cancer development lines a portion of the distal oesophagus, is the only known precursor of oesophageal adenocarcinoma, the incidence of which has increased profoundly over the past several decades. Most evidence suggests that Barrett oesophagus develops from progenitor cells at the oesophagogastric junction that proliferate and undergo epithelial-mesenchymal transition as part of a wound-healing process that replaces oesophageal squamous epithelium damaged by gastroesophageal reflux disease (GERD). GERD also seems to induce reprogramming of key transcription factors in the progenitor cells, resulting in the development of the specialized intestinal metaplasia that is characteristic of Barrett oesophagus, probably through an intermediate step of metaplasia to cardiac mucosa. Genome-wide association studies suggest that patients with GERD who develop Barrett oesophagus might have an inherited predisposition to oesophageal metaplasia and that there is a shared genetic susceptibility to Barrett oesophagus and to several of its risk factors (such as GERD, obesity and cigarette smoking). In this Review, we discuss the mechanisms, pathophysiology, genetic predisposition and cells of origin of Barrett oesophagus, and opine on the clinical implications and future research directions.

Indexed as

Barrett EsophagusEsophageal NeoplasmsGastroesophageal RefluxGenome-Wide Association StudyHumansMetaplasia

Identifiers

PMID35672395
OpenAlexW4281824536

What Socratic 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 Socratic graph.