ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Bisphenol A disrupts cartilage homeostasis through CYP2C19.
Article in Naunyn-Schmiedeberg's archives of 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.
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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.
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Authors and funding
5 authors.
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Abstract
Bisphenol A (BPA), a ubiquitous endocrine-disrupting chemical (EDC), disrupts hormonal signaling and induces inflammation, yet its role in osteoarthritis (OA) pathogenesis remains unclear, underscoring a critical environmental health research gap. We employed network toxicology and molecular docking techniques to analyze BPA's interactions with OA-associated protein targets. Key genes were identified through multi-database integration and prioritized using topological metrics (degree/betweenness/closeness centrality). Enrichment analysis (GO/KEGG) was conducted to map biological pathways. At the same time, AutoDock Vina evaluated the binding affinities of three compounds (BPA, the OA treatment drug abiraterone retrieved from DrugBank, and the OA modeling agent iodoacetic acid) with core targets. Integrated analysis identified 233 shared BPA-OA targets. Enrichment analysis revealed that BPA perturbs extracellular matrix (ECM) organization (p = 3.2 × 10⁻
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