ArticleFrontiers in endocrinology2025
Elucidating the mechanism of triphenyl phosphate interference in bone metabolism via network toxicology and molecular docking methodologies.
Article in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Network toxicology deciphers micro- and nanoplastics-mediated mixture hazard, predictive risk assessment, and regulatory translation.Archives of toxicology · 2026Review
- Zebrafish as a Model Organism to Study Neurotoxicity: A Potential Tool for Neuroprotective Drug Discovery.Current drug metabolism · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study aims to elucidate the molecular mechanisms by which the widely used organophosphate flame retardant and plasticizer, triphenyl phosphate (TPhP), disrupts bone metabolism, highlighting the potential impact of environmental chemicals on bone homeostasis. Methods: A combined approach of network toxicology and molecular docking was employed to investigate the molecular mechanisms underlying the effects of TPhP on bone metabolism. Potential targets associated with both TPhP and bone metabolism were identified through database searches in ChEMBL, STITCH, GeneCards, and OMIM. A protein-protein interaction (PPI) network was constructed using the STRING database and analyzed with Cytoscape software. Functional enrichment analyses, including Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, were performed to determine the major pathways involved. Molecular docking was conducted to evaluate the binding affinity between TPhP and key target proteins. Additionally, Results: 78 potential targets related to both TPhP and bone metabolism were identified. STRING and Cytoscape revealed six key proteins: IGF1R, NR3C1, MAP3K1, BRAF, WNK4, and CNR2. GO and KEGG analyses indicated that these targets predominantly function through the MAPK signaling pathway. Molecular docking results demonstrated strong binding affinities between TPhP and key targets, particularly BRAF and WNK4. Conclusion: TPhP disrupts bone metabolism by modulating key proteins and pathways, underscoring its potential health risks and the need for further epidemiological and clinical research.
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