ArticleFrontiers in nutrition2026
Elucidating the therapeutic mechanisms of quercetin in hepatic fibrosis: an integrated metabolomic and transcriptomic analysis.
Article in Frontiers in nutrition, 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Combined metabolomics and transcriptomics analyses were performed to elucidate metabolites related to quercetin (Que) treatment in rats with CCl₄-induced hepatic fibrosis (HF). Methods: Histopathology, hepatic inflammatory and fibrosis-related markers, and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) were used to profile fibrosis-associated changes. Results: QUE treatment was associated with altered whole-liver expression of lipid metabolism genes (Cpt1a, Acadm, Hadh, and Scd). Nevertheless, because the analyzed datasets were derived from the whole liver, these changes could not be mapped to their cellular source. Correspondingly, QUE treatment was associated with changes in arachidonic acid, hydroxyacyl-coenzyme A (CoA), β-hydroxybutyrate, and leukotriene A4. The aforementioned metabolites were enriched in fatty acid oxidation (FAO), arachidonic acid metabolism, ketone body biosynthesis, endoplasmic reticulum stress, and retinol metabolism. Conclusion: In summary, QUE treatment was associated with attenuation of hepatic fibrosis and lipid-energy metabolism-related changes. Due to the inability of bulk liver transcriptomic analyses to distinguish hepatocyte-derived changes from hepatic stellate cell (HSC)-derived changes, the restoration of Cpt1a should be interpreted as a whole-liver metabolic association rather than cell-specific antifibrotic evidence until further studies can validate this association.
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.