Authors
Yinpei Tang, Linjing She, Yaping Sun, Zhengwang Zhu, Pingsheng Zhu
Published in
Toxicology reports. Volume 17. Pages 102167. Epub Nov 15, 2025.
Abstract
Bisphenol A (BPA), a widespread environmental endocrine-disrupting chemical, is suspected to contribute to liver injury, yet the underlying mechanisms, particularly for cholestatic liver injury (CLI), remain poorly defined. This study aims to systematically elucidate the molecular pathways by which BPA induces CLI.
We applied an integrated network toxicology approach. BPA targets were predicted using chemical databases (ChEMBL, SwissTargetPrediction, TargetNet), while disease targets for CLI were sourced from GeneCards and OMIM. Bioinformatics analyses, including Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, were conducted on overlapping genes. A protein-protein interaction network was constructed to identify hub genes, followed by molecular docking simulations to validate BPA's binding affinity to these key targets.
We identified 200 common genes linking BPA exposure to CLI. Pathway analysis revealed that BPA perturbs multiple biological processes, including chemical detoxification, energy metabolism, inflammation, and bile secretion. Ten core genes (TP53, TNF, and key CYP450 enzymes) were pinpointed as central players. Molecular docking confirmed that BPA binds strongly to these hub targets, substantiating their mechanistic role.
Our findings provide a comprehensive mechanistic framework explaining how BPA exposure may lead to cholestatic liver injury. The study establishes a novel predictive strategy for evaluating the hepatotoxicity of environmental pollutants.
PMID:
42437265
Bibliographic data and abstract were imported from PubMed on 12 Jul 2026.
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