ArticleScientific reports2025
The effect of phytoestrogens and PAHs on endometriosis and the involvement of gut microbiota, inflammation, and molecular targets.
Article in Scientific reports, 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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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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Who cites it
2 citing papers in PubMed.
- Endometriosis: Epidemiology, Risk Factors, Molecular Mechanisms, Diagnosis, and Management.MedComm · 2026Review
- Associations between aggregate index of systemic inflammation and endometriosis risk utilizing logistic regression analysis.Frontiers in medicine · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Endometriosis is a common estrogen-dependent inflammatory disease, yet its complex etiology is not fully understood. Endocrine Disrupting Chemicals (EDCs) exposure disrupts human reproduction, but studies on mixed EDCs and endometriosis risk are Limited. The study Analyzed 2,644 women, assessing 12 phthalates, 8 polycyclic aromatic hydrocarbons, And 6 phytoestrogens in a representative US population. Various statistical models (generalized linear model, partial least squares discriminant analysis, weighted quantile sum, quantile g-computation, restricted cubic spline) were used to explore the link between EDC exposure and endometriosis risk, with mediating effects of lipid metabolism and inflammatory biomarkers examined. Biological mechanisms were identified through an integrated strategy involving target analysis of key chemicals and endometriosis intersections, network establishment, pathway analysis, and target validation. Various statistical models revealed that the gut microbiota metabolite enterolactone (ENL) was negatively associated with endometriosis, while the PAH metabolite 1-Hydroxyphenanthrene (1-OHPHE) was positively associated. Mediation analysis showed that uric acid (UA) and ferritin (Fer) were associated with mediating pathways in the relationships between ENL And decreased risk, And 1-OHPHE and increased risk, respectively. Network and target analysis indicated that ENL affects risk via ESR1, while 1-OHPHE disturbs it through GRB2. ENL can bind to XDH, inhibiting UA production. ENL supplementation may mitigate PAH-induced risks through the PI3K-Akt pathway. In conclusion, higher ENL levels were associated with reduced endometriosis risk, while 1-OHPHE was associated with increased prevalence. Inflammatory mediators UA And Fer demonstrated potential mediating associations in these relationships. ENL levels may be associated with attenuation of 1-OHPHE associations with endometriosis, potentially through gut microbiota-related pathways. These findings emphasize the role of environmental and microbiome interactions in modulating endometriosis risk.
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