Evidence map›Paper›PMID 30831083›Full record

ReviewGastroenterology2019

Gastric Parietal Cell Physiology and Helicobacter pylori-Induced Disease.

Xuebiao Yao, Adam J Smolka

Open access · bronzeAbstract readReview
In one paragraph

Review in Gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
13.3field-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

70 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Review
  3. Pan-tissue transcriptomic profiling of dairy cattle.Journal of animal science and biotechnology · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. The Potential Role ofMicroorganisms · 2025
    Review
  10. Review
  11. Review
  12. Standard: Human gastric organoids.Cell regeneration (London, England) · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

10 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

2 authors at 2 institutions in 2 countries.

Xuebiao YaoMOE Key Laboratory of Cellular Dynamics, CAS Center for Excellence in Molecular Cell Science, University of Science and Technology of China, Hefei, China; Keck Center for Cellular Dynamics and Organoids Plasticity, Morehouse School of Medicine, Atlanta, Georgia. Electronic address: yaoxb@ustc.edu.cn.
Adam J SmolkaGastroenterology and Hepatology Division, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina.
Medical University of South Carolina · USUniversity of Science and Technology of China · CN

Funding

The function of ezrin in stimulus-coupled acid secretionR01DK056292 · NIDDK · UNIVERSITY OF WISCONSIN MADISON · PI YAO, XUEBIAO · 1999 to 2012
$2.5M
Function of ACAP4 in CCL18-stimulated breast cancer metastasisR01CA164133 · NCI · MOREHOUSE SCHOOL OF MEDICINE · PI YAO, XUEBIAO · 2012 to 2016
$1.4M
Mechanisms of H pylori-Induced HypochlorhydriaR01DK064371 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SMOLKA, ADAM J · 2005 to 2008
$1.0M
FUNCTION OF MST4-EZRIN-ACAP4 SIGNALING IN GASTRIC PARIETAL CELL SECRETION AND HOMEOSTASISR01DK115812 · NIDDK · MOREHOUSE SCHOOL OF MEDICINE · PI YAO, XUEBIAO · 2017 to 2019
$967k
Mechanisms of H. pylori-Induced HypochlorhydriaR56DK064371 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SMOLKA, ADAM J · 2010 to 2010
$420k
NCI NIH HHS R01 CA164133NIDDK NIH HHS R01 DK056292NIDDK NIH HHS R01 DK064371NIDDK NIH HHS R01 DK115812NIDDK NIH HHS R56 DK064371
6 · The paper itself

Abstract

Acidification of the gastric lumen poses a barrier to transit of potentially pathogenic bacteria and enables activation of pepsin to complement nutrient proteolysis initiated by salivary proteases. Histamine-induced activation of the PKA signaling pathway in gastric corpus parietal cells causes insertion of proton pumps into their apical plasma membranes. Parietal cell secretion and homeostasis are regulated by signaling pathways that control cytoskeletal changes required for apical membrane remodeling and organelle and proton pump activities. Helicobacter pylori colonization of human gastric mucosa affects gastric epithelial cell plasticity and homeostasis, promoting epithelial progression to neoplasia. By intervening in proton pump expression, H pylori regulates the abundance and diversity of microbiota that populate the intestinal lumen. We review stimulation-secretion coupling and renewal mechanisms in parietal cells and the mechanisms by which H pylori toxins and effectors alter cell secretory pathways (constitutive and regulated) and organelles to establish and maintain their inter- and intracellular niches. Studies of bacterial toxins and their effector proteins have provided insights into parietal cell physiology and the mechanisms by which pathogens gain control of cell activities, increasing our understanding of gastrointestinal physiology, microbial infectious disease, and immunology.

Indexed as

Anti-Bacterial AgentsFemaleGastric MucosaGastrointestinal MicrobiomeHelicobacter InfectionsHelicobacter pyloriHumansMaleParietal Cells, GastricPrecancerous ConditionsPrognosisRisk AssessmentStomach NeoplasmsTreatment OutcomeAnti-Bacterial AgentsAcid SecretionBacteriaGastric OrganoidsH pyloriSyntelin

Identifiers

PMID30831083
PMCPMC6715393
OpenAlexW2918315477

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.