ArticleJournal of translational medicine2025
Single-cell profiling reveals a reduced epithelial defense system, decreased immune responses and the immune regulatory roles of different fibroblast subpopulations in chronic atrophic gastritis.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Review
- Exploring the High-Risk Factors of Gastric "Inflammatory Cancer Transformation" Based on Inflammatory Immune Response: Construction of RHPI Complicated With CAG Risk Prediction Model.Cancer medicine · 2026Article
- The LGR5/TFF2 ratio as a stem cell biomarker predicts high-risk status in chronic atrophic gastritis: a retrospective cohort study.BMC gastroenterology · 2026Article
- Patient-derived organoids in gastric cancer: bridging the tumor microenvironment to functional precision oncology.Frontiers in bioengineering and biotechnology · 2026Review
- Screening and functional validation of key genes inFrontiers in immunology · 2026Article
- From inflammation to carcinogenesis: MiRNA regulates epithelial-mesenchymal transition to facilitate malignant progression of gastric precancerous lesions.Frontiers in oncology · 2026Review
- Gastric organoids: A promising model for studying "inflammation-cancer" transition in atrophic gastritis.World journal of clinical oncology · 2025Review
- Overcoming diagnostic pitfalls in primary gastric squamous cell carcinoma: the imperative of adequate sampling in an elderly female patient, case report.Frontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo identify key cellular changes and molecular events in atrophic mucosa, we aimed to elucidate the molecular mechanisms driving the occurrence of chronic atrophic gastritis (CAG).
methodsWe used single-cell RNA sequencing (scRNA-seq) to characterize changes in the epithelial state and tissue microenvironment associated with CAG. The molecular changes were identified by comparing differentially expressed genes (DEGs) between the two mucosa states. Gene Ontology (GO) pathway enrichment analysis was used to explore the potential functional changes in each cell subtype in atrophic mucosa. Gene set score analysis was conducted to compare the functional roles of different fibroblast subtypes and functional changes in cell subtypes between the CAG and control groups. Metabolic analysis was performed to compare the metabolic activity of C1Q
resultsWe generated a single-cell transcriptomic atlas from 3 CAG biopsy samples and paired adjacent normal tissues. Our analysis revealed that chief cells and parietal cells exhibited a loss of detoxification ability and that surface mucous cells displayed a reduced antimicrobial defense ability in CAG lesions. The mucous neck cells in CAG lesions showed upregulation of genes related to cell cycle transition, which may lead to aberrant DNA replication. Additionally, cells with the T exhaustion phenotype infiltrated under CAG condition. C1Q
conclusionsThe main goal of this study was to comprehensively elucidate the cellular changes in CAG lesions. We observed an immune decline in the mucosal microenvironment during the development of CAG, including a reduced immune response of C1Q
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