ArticleJournal of translational medicine2026
A single-cell multi-omics atlas defines the cellular and molecular landscape of gastric intestinal metaplasia.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
16 authors.
Funding
Abstract
backgroundGastric intestinal metaplasia (GIM) is a precancerous lesion closely associated with gastric cancer (GC) risk. A systematic characterization of the molecular profiles across distinct cell types during GIM progression is crucial for devising new intervention strategies and enabling early prevention for GC.
methodsThis study integrates single-cell transcriptomics and proteomics data from gastric tissues of patients with mild chronic non-atrophic gastritis (CNAG) and moderate-to-severe GIM.
resultsWe identified differentially expressed genes (DEGs) and proteins (DEPs) that show consistent changes at both transcriptional and protein levels across epithelial, stromal, and immune cells. Notably, most proteins were downregulated in GIM tissues, potentially linked to reduced expression of RNA splicing-related genes. Epithelial cells in GIM lesions exhibited intestinal-type subpopulations, including goblet and enterocytes, likely originating from gastric isthmus stem cells. Despite overall protein downregulation, the ubiquitin-like protein NEDD8 was markedly upregulated in metaplastic tissues, especially in H. pylori-positive tissues. Pathways involved in cytoskeleton maintenance, extracellular matrix stability, and cell adhesion were downregulated, while several macrophage-expressed DEGs/DEPs (e.g., BST2, CYBB, ITGB2) were elevated.
conclusionsThis work delineates dynamic transcriptional and translational alterations during the progression from mild gastritis to GIM. It implies that chronic inflammatory injury causes suppress protein synthesis, further driving metaplastic transformation early gastric precancerous lesions.
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