Evidence map›Paper›PMID 32755448›Full record

ReviewAmerican journal of physiology. Cell physiology2020

Role of metaplasia during gastric regeneration.

Emma Teal, Martha Dua-Awereh, Sabrina T Hirshorn, Yana Zavros

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Protective effect of magnesium on indomethacin-induced gastric ulcer in mice.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. An antibiotic-free platform for eliminating persistentActa pharmaceutica Sinica. B · 2024
    Article
  10. Article
  11. Review
  12. SOX9 Governs Gastric Mucous Neck Cell Identity and Is Required for Injury-Induced Metaplasia.Cellular and molecular gastroenterology and hepatology · 2023
    Article
  13. The immune microenvironment in gastric adenocarcinoma.Nature reviews. Gastroenterology & hepatology · 2022
    Review
  14. Review
  15. Gastric epithelial histology and precancerous conditions.World journal of gastrointestinal oncology · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. 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

4 authors at 2 institutions in 1 country.

Emma TealDepartment of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Martha Dua-AwerehDepartment of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Sabrina T HirshornDepartment of Cellular and Molecular Medicine, University of Arizona College of Medicine, Tucson, Arizona.
Yana ZavrosDepartment of Cellular and Molecular Medicine, University of Arizona College of Medicine, Tucson, Arizona.
University of Arizona · USUniversity of Cincinnati Medical Center · US

Funding

The role of Hedgehog Signaling in gastric tissue repair and regenerationR01DK083402 · NIDDK · UNIVERSITY OF CINCINNATI · PI ZAVROS, YANA · 2011 to 2019
$3.7M
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R01DK083402-08NIDDK NIH HHS R01 DK083402
6 · The paper itself

Abstract

Spasmolytic polypeptide/trefoil factor 2 (TFF2)-expressing metaplasia (SPEM) is a mucous-secreting reparative lineage that emerges at the ulcer margin in response to gastric injury. Under conditions of chronic inflammation with parietal cell loss, SPEM has been found to emerge and evolve into neoplasia. Cluster-of-differentiation gene 44 (CD44) is known to coordinate normal and metaplastic epithelial cell proliferation. In particular, CD44 variant isoform 9 (CD44v9) associates with the cystine-glutamate transporter xCT, stabilizes the protein, and provides defense against reactive oxygen species (ROS). xCT stabilization by CD44v9 leads to defense against ROS by cystine uptake, glutathione (GSH) synthesis, and maintenance of the redox balance within the intracellular environment. Furthermore, p38 signaling is a known downstream ROS target, leading to diminished cell proliferation and migration, two vital processes of gastric epithelial repair. CD44v9 emerges during repair of the gastric epithelium after injury, where it is coexpressed with other markers of SPEM. The regulatory mechanisms for the emergence of CD44v9 and the role of CD44v9 during the process of gastric epithelial regeneration are largely unknown. Inflammation and M2 macrophage infiltration have recently been demonstrated to play key roles in the induction of SPEM after injury. The following review proposes new insights into the functional role of metaplasia in the process of gastric regeneration in response to ulceration. Our insights are extrapolated from documented studies reporting oxyntic atrophy and SPEM development and our current unpublished findings using the acetic acid-induced gastric injury model.

Indexed as

Acetic AcidAnimalsGastric MucosaHumansMetaplasiaRegenerationStomachAcetic AcidCD44 variant isoform 9cystine-glutamate transportergastric ulcersspasmolytic polypeptide-expressing metaplasia

Identifiers

PMID32755448
PMCPMC7792674
OpenAlexW3047003155

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.