ArticleCellular and molecular gastroenterology and hepatology2021
Inflammation-Associated Senescence Promotes Helicobacter pylori-Induced Atrophic Gastritis.
Article in Cellular and molecular gastroenterology and hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
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- Impact of kimura-takemoto atrophy classification on first-lineFrontiers in medicine · 2026Article
- Gastric organoids: A promising model for studying "inflammation-cancer" transition in atrophic gastritis.World journal of clinical oncology · 2025Review
- Sheng-Jiang-Yi-You decoction inhibits the inflammatory response by down-regulating the p38MAPK signaling pathway to alleviateHistology and histopathology · 2025Article
- Role of long non-coding RNAs in the pathogenesis of gastric cancer-induced by Helicobacter pylori.Inflammopharmacology · 2025Review
- DNMT1/MTTP axis promotes gastritis progression duringEpigenomics · 2025Article
- Jatrorrhizine attenuates inflammatory response in Helicobacter pylori-induced gastritis by suppressing NLRP3 inflammasomes and NF-κB signaling pathway.Archives of microbiology · 2025Article
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- Targeting B4GALT3 in BMSCs-EVs for Therapeutic Control of HCC via NF-κB pathway inhibition.Cell biology and toxicology · 2025Article
- Antibiotic resistance ofWorld journal of gastroenterology · 2025Article
- Association ofFrontiers in medicine · 2025Review
- 5-hydroxymethylcytosine signature in plasma extracellular vesicle DNA as a diagnostic molecular biomarker for precancerous lesions of gastric cancer.Extracellular vesicles and circulating nucleic acids · 2025Article
- The oral-gut axis in chronic atrophic gastritis: current perspectives and integrated strategies.Frontiers in immunology · 2025Review
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- Increased ONECUT2 induced by Helicobacter pylori promotes gastric cancer cell stemness via an AKT-related pathway.Cell death & disease · 2024Article
Corrections and comments
- Commented on by
- Erratum issuedCorrection.2024
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsThe association between cellular senescence and Helicobacter pylori-induced atrophic gastritis is not clear. Here, we explore the role of cellular senescence in H pylori-induced atrophic gastritis and the underlying mechanism.
methodsC57BL/6J mice were infected with H pylori for biological and mechanistic studies in vivo. Gastric precancerous lesions from patients and mouse models were collected and analyzed using senescence-associated beta-galactosidase, Sudan Black B, and immunohistochemical staining to analyze senescent cells, signaling pathways, and H pylori infection. Chromatin immunoprecipitation, luciferase reporter assays, and other techniques were used to explore the underlying mechanism in vitro.
resultsGastric mucosa atrophy was highly associated with cellular senescence. H pylori promoted gastric epithelial cell senescence in vitro and in vivo in a manner that depended on C-X-C motif chemokine receptor 2 (CXCR2) signaling. Interestingly, H pylori infection not only up-regulated the expression of CXCR2 ligands, C-X-C motif chemokine ligands 1 and 8, but also transcriptionally up-regulated the expression of CXCR2 via the nuclear factor-κB subunit 1 directly. In addition, CXCR2 formed a positive feedback loop with p53 to continually enhance senescence. Pharmaceutical inhibition of CXCR2 in an H pylori-infected mouse model attenuated mucosal senescence and atrophy, and delayed further precancerous lesion progression.
conclusionsOur study showed a new mechanism of H pylori-induced atrophic gastritis through CXCR2-mediated cellular senescence. Inhibition of CXCR2 signaling is suggested as a potential preventive therapy for targeting H pylori-induced atrophic gastritis. GEO data set accession numbers: GSE47797 and GSE3556.
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