Evidence map›Paper›PMID 39622791›Full record

ReviewCell death discovery2024

Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis.

Yun Liu, Renjie Miao, Jinxuan Xia, Yong Zhou, Jun Yao, Shihe Shao

Abstract readReview
In one paragraph

Review in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Molecules (Basel, Switzerland) · 2026
    Review
  3. Targeting ferroptosis inInternational journal of oncology · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Characterization ofFrontiers in microbiology · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Cancer genomics & proteomics
    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

6 authors.

Yun Liu *Department of Gastroenterology, Institute of Digestive Disease, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, Jiangsu, China.
Renjie Miao *Department of Clinical laboratory, Affiliated Third Hospital of Zhenjiang to Jiangsu University, Zhenjiang, Jiangsu, China.
Jinxuan XiaZhenjiang Mental Health Center, Jiangsu, China.
Yong ZhouDepartment of Gastroenterology, Institute of Digestive Disease, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, Jiangsu, China. 595353314@qq.com.
Jun YaoDepartment of Gastroenterology, Institute of Digestive Disease, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, Jiangsu, China. 6000003331@ujs.edu.cn.
Shihe ShaoSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China. shaoshihe2006@163.com.ORCID http://orcid.org/0000-0001-9883-772X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Helicobacter pylori (H. pylori) is a gram-negative pathogen that colonizes gastric epithelial cells, and its chronic infection is the primary risk factor for the development of gastric cancer (GC). Ferroptosis is an iron-dependent form of cell death characterized by intracellular lipid peroxide accumulation and reactive oxygen species (ROS) imbalance. There is evidence suggesting that pathogens can manipulate ferroptosis to facilitate their replication, transmission, and pathogenesis. However, the interaction between ferroptosis and H. pylori infection requires further elucidation. We reviewed the mechanism of ferroptosis and found that H. pylori virulence factors such as cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA), neutrophil-activating protein A (NapA), superoxide dismutase B (SodB), γ-glutamyl transpeptidase (gGT), lipopolysaccharide (LPS), and outer inflammatory protein A (OipA) affected glutathione (GSH), ROS, and lipid oxidation to regulate ferroptosis. It also affected the progression of GC by regulating ferroptosis-related indicators through abnormal gene expression after H. pylori infected gastric mucosa cells. Finally, we discuss the potential application value of ferroptosis inducers, inhibitors and other drugs in treating H. pylori-infected GC patients while acknowledging that their interactions are still not fully understood.

Identifiers

PMID39622791
PMCPMC11612470

What Socratic holds

Textmetadata
LicenceCC BY
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.