ArticleBMC gastroenterology2026
Citraconic acid mitigates radiation-induced intestinal injury by modulating IL-17 signaling to enhance epithelial regeneration.
Article in BMC gastroenterology, 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
4 authors.
Funding
Abstract
objectiveThis study investigates the protective effects of citraconic acid (CA) on radiation-induced intestinal injury (RIII) and elucidates its relationship with the interleukin-17 (IL-17) signaling pathway.
methodsA mouse model of whole-abdominal irradiation (IR) was established, and CA (10, 20, 40 mg/kg) was administered intraperitoneally as an intervention. Assessments included body weight, Disease Activity Index (DAI), and colon length measurements. Serum and tissue inflammatory markers were quantified using enzyme-linked immunosorbent assay. Histological analysis was performed using Hematoxylin and Eosin (HE) staining, Ki67 and Lgr5 immunohistochemistry, Alcian Blue-Periodic Acid-Schiff (AB-PAS) staining, and immunofluorescence for Zonula Occludens-1 (ZO-1) and Occludin. Transcriptomic sequencing with functional enrichment analyses was conducted, followed by Western blot validation of IL-17 A, CCL7, CXCL2, and MMP13 protein expression. IL-17 inhibitor experiments were performed to validate the causal relationship.
resultsCA administration attenuated body weight loss and reduced DAI scores in a dose-dependent manner while preserving colon length. CA treatment suppressed the elevation of IL-6 and TNF-α levels induced by irradiation. Furthermore, CA enhanced the abundance of Ki67-positive and Lgr5-positive cells, increased goblet cell numbers and mucus secretion, and restored the expression of tight junction proteins ZO-1 and Occludin, thereby improving histological damage. Transcriptomic analysis revealed significant enrichment of IL-17 signaling pathways associated with regeneration and inflammation. Protein levels of IL-17 A, CCL7, CXCL2, and MMP13 were upregulated following CA treatment. Importantly, IL-17 inhibition abolished the protective effects of CA, confirming the dependence on IL-17 signaling.
conclusionCA exerts protective effects against radiation-induced intestinal injury by modulating the IL-17-related signaling network, thereby promoting intestinal epithelial regeneration and barrier repair. These findings suggest that CA may represent a potential metabolic intervention strategy for the prevention and treatment of radiation-induced gastrointestinal damage.
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.