ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2010
Helicobacter pylori: a ROS-inducing bacterial species in the stomach.
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
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.
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.
Who cites it
113 citing papers in PubMed, 209 citations in OpenAlex.
- Increased protein carbonylation and decreased antioxidant status in anemic H. pylori infected patients: effect of treatment.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationTrial
- Exploring the Multifunctional Benefits of Astaxanthin in Aging, Oxidative Stress, Immune Dysfunction, Gut and Skin Health.Antioxidants (Basel, Switzerland) · 2026Review
- TheJournal of bacteriology · 2026Article
- From gut to mouth: salivary signatures of carcinogenic microbiota.Frontiers in cellular and infection microbiology · 2026Review
- A Narrative Review on Unravelling Bacterial-Mediated Carcinogenesis and Possible Alternative Treatment Strategies.BioMed research international · 2026Review
- Pathogenicity and virulence ofVirulence · 2025Review
- Metformin Inhibits the Development of Helicobacter pylori-Associated Gastritis by Regulating the ERK-MMP10-IL-1β Axis.Cell biochemistry and biophysics · 2025Article
- Plant-derived extracts or compounds for Helicobacter-associated gastritis: a systematic review of their anti-Helicobacter activity and anti-inflammatory effect in animal experiments.Chinese medicine · 2025Review
- Bacterial small molecule metabolites implicated in gastrointestinal cancer development.Nature reviews. Microbiology · 2025Review
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- Unravelling Peptic Ulcers: Comprehensive Insights into Etiology, Diagnosis, Screening Techniques, and Treatment.Current pharmaceutical design · 2025Review
- Targeting the DNA damage response (DDR) of cancer cells with natural compounds derived fromJournal of ginseng research · 2025Review
- Gastrointestinal cancer resistance to treatment: the role of microbiota.Infectious agents and cancer · 2024Review
- Mechanistic Insights on Microbiota-Mediated Development and Progression of Esophageal Cancer.Cancers · 2024Review
- ROS-mediated up-regulation of SAE1 by Helicobacter pylori promotes human gastric tumor genesis and progression.Journal of translational medicine · 2024Article
- IL-33 Accelerates Chronic Atrophic Gastritis through AMPK-ULK1 Axis Mediated Autolysosomal Degradation of GKN1.International journal of biological sciences · 2024Article
- Tryptophan Metabolism in Obesity: The Indoleamine 2,3-Dioxygenase-1 Activity and Therapeutic Options.Advances in experimental medicine and biology · 2024Review
- Copper-Bearing Metal-Organic Framework with Mucus-Penetrating Function for the Multi-Effective Clearance of Mucosal ColonizedResearch (Washington, D.C.) · 2024Article
- Review
- Diversification and deleterious role of microbiome in gastric cancer.Cancer reports (Hoboken, N.J.) · 2023Review
53 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundReactive oxygen species (ROS) and reactive nitrogen species (RNS) have been reported to impact gastric inflammation and carcinogenesis. However, the precise mechanism by which Helicobacter pylori induces gastric carcinogenesis is presently unclear.
aimThis review focuses on H. pylori-induced ROS/RNS production in the host stomach, and its relationship with gastric carcinogenesis.
resultsActivated neutrophils are the main source of ROS/RNS production in the H. pylori-infected stomach, but H. pylori itself also produces ROS. In addition, extensive recent studies have revealed that H. pylori-induced ROS production in gastric epithelial cells might affect gastric epithelial cell signal transduction, resulting in gastric carcinogenesis. Excessive ROS/RNS production in the stomach can damage DNA in gastric epithelial cells, implying its involvement in gastric carcinogenesis.
conclusionUnderstanding the molecular mechanism behind H. pylori-induced ROS, and its involvement in gastric carcinogenesis, is important for developing new strategies for gastric cancer chemoprevention.
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What OpenQuestion holds
Registered trials
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.