ArticleJournal of ovarian research2026
Bisphenol a and polycystic ovary syndrome in reproductive-age women: mechanistic exploration via network toxicology and molecular docking.
Article in Journal of ovarian research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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
1 citing paper in PubMed.
- A network toxicology and machine learning approach to uncover the molecular machinery of bisphenol A-induced colorectal cancer.Scientific reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Polycystic Ovary Syndrome (PCOS) is a prevalent endocrine and metabolic disorder affecting 6–20% of reproductive-age women worldwide, characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology, often accompanied by insulin resistance and infertility. Emerging evidence suggests that environmental endocrine-disrupting chemicals, such as Bisphenol A (BPA), may contribute to PCOS pathogenesis. This study employs network toxicology and molecular docking to elucidate the mechanistic links between BPA exposure and PCOS. By integrating multi-database analyses, we identified 294 BPA-related targets and 67 shared targets with PCOS, including key genes (PPARG, HSP90AA1, IGF1R, and INSR) implicated in hormonal dysregulation, insulin resistance, and inflammation. Protein-protein interaction (PPI) networks and enrichment analyses revealed their involvement in critical pathways such as estrogen signaling, ovarian steroidogenesis, and PI3K-Akt signaling. Molecular docking confirmed stable binding between BPA and these targets, with IGF1R exhibiting the strongest affinity (− 8.0 kcal/mol). Validation using the GSE5090 dataset demonstrated significant upregulation of PPARG and HSP90AA1 in PCOS patients. Our findings suggest that BPA disrupts follicular development, exacerbates hyperandrogenism, and impairs metabolic homeostasis through multi-target interactions, providing novel insights into the environmental etiology of PCOS and potential therapeutic strategies.
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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.