ArticleFrontiers in immunology2026
EPS deficiency aggravates intestinal mucosal inflammation and dysbiosis through disrupting macrophage polarization balance in ulcerative colitis.
Article 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ulcerative colitis (UC) is a chronic, immune-mediated inflammatory bowel disorder, and macrophages are essential for maintaining intestinal mucosal balance during UC. Long intergenic non-coding RNA-erythroid prosurvival (lincRNA-EPS) is a novel lincRNA identified as a key inflammatory regulator. Nonetheless, the specific role of EPS in the pathogenesis of UC remains unclear. Methods: To investigate the contribution of EPS to intestinal inflammation, a model of colitis induced by dextran sulfate sodium (DSS) was created using both EPS gene knockout (EPS Results: EPS Conclusions: This study revealed a novel function of EPS in macrophages in regulating the M1/M2 balance, inflammation, and gut microbiota during the pathological process of UC, and targeting EPS may represent a promising therapeutic approach for UC.
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.