ArticleFrontiers in pharmacology2025
Temporal metabolic reprogramming in DSS-induced colitis identifies purine metabolism and trigonelline as novel therapeutic targets.
Article in Frontiers in pharmacology, 2025. 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
Background: Inflammatory bowel disease (IBD) is a multifactorial disorder characterized by aberrant immune activation and metabolic dysregulation. Despite significant advances in understanding immune mechanisms, the temporal dynamics of metabolic alterations during intestinal inflammation and their therapeutic implications remain poorly defined. Methods: To investigate metabolic reprogramming during colitis progression, we conducted time-resolved metabolomic profiling of the colon, mesenteric lymph nodes (MLNs), and serum in a dextran sulfate sodium (DSS)-induced murine colitis model at days 1, 3, 5, and 7 post-induction. Targeted and untargeted metabolomic analyses were integrated with pathological and immunological assessments. To assess therapeutic relevance, DSS-treated mice were administered either trigonelline, a metabolite identified in serum, or mycophenolic acid (MPA), a purine metabolism inhibitor, separately. Metabolomic profiling revealed a progressive activation of purine metabolism in colonic tissues and MLNs, correlating with enhanced immune-inflammatory responses. Results: Trigonelline was identified as a serum biomarker positively associated with disease severity. Therapeutic treatment with either trigonelline or MPA significantly alleviated histopathological damage, reduced inflammatory cell infiltration in both the colon and MLNs, and restored the Th17/Treg cell balance. Mechanistic studies indicated that trigonelline and MPA individually suppress pro-inflammatory signaling pathways while promoting regulatory immune responses. Conclusion: This study provides a comprehensive temporal map of metabolic reprogramming during colitis progression and identifies purine metabolism and trigonelline as novel therapeutic targets. These findings highlight the translational potential of multi-organ metabolomic approaches in elucidating disease mechanisms and guiding precision treatment strategies for IBD and related inflammatory conditions.
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.