Shared molecular mechanisms of bisphenol A and phthalates in endometriosis: A bioinformatics and molecular docking study

Shared molecular mechanisms of bisphenol A and phthalates in endometriosis: A bioinformatics and molecular docking study

Objective: Emerging evidence links endometriosis with co-exposure to Bisphenol A (BPA) and phthalates; however, their combined toxicogenomic mechanisms remain unclear. This study investigated the shared molecular pathways of BPA and phthalates—Diethyl phthalate (DEP), Dimethyl phthalate (DMP), and D...

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Bibliographic Details
Main Authors: Zhixiang Fan, Reyilanmu Maisaidi, Yibanuer Reheman, Yang Li, Penglai Zhou, Lili Han
Format: Article
Language:English
Published: Elsevier 2025-07-01
Series:Ecotoxicology and Environmental Safety
Subjects:
Bisphenol A
Phthalates
Bioinformatics
Endometriosis
Molecular Docking
Online Access:http://www.sciencedirect.com/science/article/pii/S0147651325007249
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Summary:Objective: Emerging evidence links endometriosis with co-exposure to Bisphenol A (BPA) and phthalates; however, their combined toxicogenomic mechanisms remain unclear. This study investigated the shared molecular pathways of BPA and phthalates—Diethyl phthalate (DEP), Dimethyl phthalate (DMP), and Dioctyl phthalate (DOP)—in endometriosis pathogenesis. Methods: Bioinformatics and molecular docking analyses were integrated to characterize the chemical-pathway interactions in endometriosis development. Results: We identified 81 shared targets of BPA/phthalates associated with endometriosis. Functional enrichment revealed their involvement in estrogen signaling, oxidative stress, inflammation, and cell proliferation/migration. PPI network analysis prioritized four hub targets (HSP90AA1, AKT1, SRC, IGF1) validated in endometriotic lesions and functionally linked to PI3K-Akt signaling and a dual hyperinflammatory-immunosuppressive imbalance. Molecular docking demonstrated that BPA and phthalates bind these proteins at shared sites, suggesting mechanistic convergence. Conclusion: BPA and phthalates co-promote endometriosis through overlapping signaling pathways. These findings provide mechanistic insights into their combined effects and establish a framework for understanding environmental chemical synergism in disease etiology.
ISSN:0147-6513

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