ArticleFrontiers in pharmacology2026
Mechanism of BaP- regulated hepatic lipid metabolism via AhR activation and AR modulation.
Article in Frontiers in pharmacology, 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
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Benzo[a]pyrene (BaP) is a ubiquitous environmental pollutant that disturbs hepatic lipid metabolism. The androgen receptor (AR) protects hepatic lipid homeostasis, but whether BaP interferes with AR nuclear translocation through aryl hydrocarbon receptor (AhR) activation to cause metabolic disorders remains unknown Methods: An androgen-deficient mouse model was established by bilateral orchiectomy, and lipid disorders were induced by BaP (0.9 mg kg Results: In androgen-present mice, BaP induced liver injury and lipid accumulation, inhibited AR nuclear translocation, reduced β-oxidation genes (PGC-1α, CPT1A, PPARα), and increased lipogenic genes (SREBP2, HMGCR, LXRα). In androgen-deficient mice, BaP promoted AR translocation and improved lipid metabolism. In HepG2 cells, BaP alone enhanced AR translocation and fatty acid oxidation, while BaP + DHT inhibited AR translocation and promoted lipogenesis. All effects were reversed by CH223191. Conclusion: BaP exerts bidirectional regulation on AR via AhR: it exerts an anti-androgenic in androgen-replete conditions and regulates AR-related signaling pathways in androgen deficiency. The AhR-AR axis is a key target for preventing BaP-induced hepatic steatosis.
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.