ReviewBiochemistry and biophysics reports2026
Epigenetic regulation by gut microbiota-derived metabolites in celiac disease.
Review in Biochemistry and biophysics reports, 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Celiac disease (CeD) is a chronic autoimmune disorder triggered by gluten in genetically susceptible individuals carrying HLA-DQ2/DQ8 haplotypes. Although genetic predisposition and gluten exposure are necessary, they are insufficient in the development of the disease, pointing to critical roles for environmental factors-particularly gut microbiota dysbiosis and its metabolites-in disrupting immune tolerance through epigenetic mechanisms. This review collects current evidence on the microbiota-metabolite-epigenetic axis in CeD pathogenesis. Dysbiosis is characterized by reduced microbial diversity, depletion of protective taxa (e.g., Bacteroidetes), and enrichment of pro-inflammatory groups. Bacterial metabolites exert opposing effects: short-chain fatty acids (SCFAs), especially butyrate, act protectively by inhibiting histone deacetylases, promoting histone acetylation, stabilizing anti-inflammatory FOXP3 isoforms in regulatory T cells, and modulating alternative splicing and miRNA networks to reinforce barrier integrity and immune tolerance. Conversely, certain metabolites and microbial signals can drive pathogenic epigenetic changes, including altered DNA methylation, histone modifications, and miRNA dysregulation that amplify NF-κB, IL-17, and IFN-γ pathways. Emerging data from organoid models and multi-omics studies further highlight the therapeutic potential of microbial-derived postbiotics and cell-free supernatants (e.g., from
Indexed as
Identifiers
What Socratic 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 Socratic graph.