ReviewFrontiers in immunology2026
Exosome-mediated metabolic-immune regulatory axis: mechanisms of gastric cancer progression and resistance and targeting strategies.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) is characterized by marked heterogeneity and frequent resistance to chemotherapy and immunotherapy. Exosomes mediate intercellular communication between tumor, stromal, and immune cells and may couple metabolic adaptation to immune suppression. This review synthesizes evidence for a bidirectional exosome-mediated metabolic-immune axis in GC. Tumor-derived exosomes enhance glycolytic and other metabolic programs, remodel macrophage and lymphocyte function, and promote immune escape, metastasis, and treatment resistance. Conversely, exosomes released by cancer-associated fibroblasts, tumor-associated macrophages, and mesenchymal stromal cells reinforce tumor-cell metabolism, stemness, survival, and chemoresistance. Together, these reciprocal interactions form a self-reinforcing circuit that links metabolic plasticity with an immunosuppressive microenvironment. We further evaluate circulating exosomal cargoes as candidate biomarkers for liquid biopsy and discuss therapeutic approaches involving inhibition of exosome biogenesis or uptake, combined metabolic and immune targeting, and engineered exosome delivery. Finally, we emphasize the limitations imposed by model systems, extracellular-vesicle heterogeneity, incomplete cell-type specificity, and inconsistent isolation and characterization methods. Defining reproducible, subtype-specific exosome-mediated interactions will be essential for translating this framework into clinically useful biomarkers and therapeutic strategies.
Indexed as
Identifiers
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.