ArticleWorld journal of gastroenterology2025
Growth differentiation factor 15 alters intestinal barrier and increases permeability: A new molecular target in inflammatory bowel disease.
Article in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- The gut-liver axis in drug-induced liver injury (DILI): Interplay between gut microbiota, intestinal barrier, and immune system.Acta pharmaceutica Sinica. B · 2026Review
- Growth differentiation factor 15 - a new molecular target in inflammatory bowel disease: Progress and challenges.World journal of gastroenterology · 2026Article
- The Microbiome-Mitochondria Axis in aging: a self-reinforcing vicious cycle linking metabolic dysregulation, mitochondrial quality control failure, and inflammaging.Frontiers in microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammatory bowel disease (IBD) is a group of chronic, inflammatory disorders that include Crohn's disease and ulcerative colitis. IBD arises from the interaction of various environmental and genetic factors. Altered gut permeability and mitochondrial stress in the colonic mucosa are two mechanisms previously implicated in IBD pathogenesis. We have previously demonstrated activation of the mitochondrial unfolded protein response (UPR
aimTo investigate whether GDF15 has a role in IBD and how GDF15 impacts colonic epithelium.
methodsCirculating levels of GDF15 were assessed in plasma samples from IBD patients and healthy controls using an enzyme-linked immunosorbent assay. To study the effects of GDF15 on the colonic mucosa, we employed two different
resultsWe found that circulating GDF15 Levels were elevated in IBD patients and correlated with markers of inflammation (C-reactive protein) and intestinal permeability [haptoglobin and lipopolysaccharide-binding protein (LBP)]. Additionally, we demonstrated that GDF15 alters the intestinal barrier and increases permeability by decreasing the levels of zonula occludens 1 and claudin 1, critical components of tight junctions. Thus, our findings confirm previous reports of increased circulating GDF15 levels in IBD patients and the activation of UPR
conclusionIn the present study, we describe a novel mechanism in IBD pathophysiology, linking mitochondrial stress to the disruption of the intestinal barrier and increased intestinal permeability.
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.