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Background <p>Triclosan, a widely used environmental contaminant with endocrine-disrupting properties, has been increasingly implicated in female reproductive disorders. However, the potential mechanistic link between triclosan exposure and endometriosis remains poorly understood.</p> Methods <p>An integrative strategy combining network toxicology, Mendelian randomization (MR), and molecular docking was applied to explore the potential mechanistic association between triclosan and endometriosis. Toxicity and ADMET profiling of triclosan were performed using ProTox-3.0 and ADMETlab 2.0. Target prediction was conducted via STITCH and SwissTargetPrediction, while endometriosis-related genes were obtained from GeneCards, OMIM, and TTD. Common targets were subjected to PPI network construction and GO/KEGG enrichment analysis. MR analysis was performed to evaluate causality between IL1B expression and endometriosis risk. Molecular docking was used to validate the binding potential of triclosan to key proteins.</p> Results <p>A total of 19 overlapping genes were identified between triclosan- and endometriosis-related targets. PPI network analysis revealed IL1B, SRC, EGFR, and KDR as hub genes. Enrichment analysis indicated significant involvement in MAPK signaling, VEGF signaling, and endocrine-related pathways. MR analysis supported a potential causal relationship between IL1B and endometriosis (MR-Egger OR = 2.66, <i>P</i> &lt; 0.05). Docking simulations demonstrated stable binding of triclosan to all four hub targets, with binding energies ranging from − 5.3 to − 5.9&#xa0;kcal/mol.</p> Conclusion <p>This study provides mechanistic insights into the potential role of triclosan in endometriosis development, highlighting IL1B as a possible causal mediator. These findings contribute to a better understanding of environmental risk factors in endometriosis and offer potential molecular targets for future research.</p>

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Mechanistic decoding of triclosan-induced endometriosis via network toxicology, Mendelian randomization, and molecular docking

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月14日

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  • Bihong Xu,
  • Maoqing Li,
  • Xiaodong Zhao,
  • Yu Qin,
  • Ying Zhao

摘要

Background

Triclosan, a widely used environmental contaminant with endocrine-disrupting properties, has been increasingly implicated in female reproductive disorders. However, the potential mechanistic link between triclosan exposure and endometriosis remains poorly understood.

Methods

An integrative strategy combining network toxicology, Mendelian randomization (MR), and molecular docking was applied to explore the potential mechanistic association between triclosan and endometriosis. Toxicity and ADMET profiling of triclosan were performed using ProTox-3.0 and ADMETlab 2.0. Target prediction was conducted via STITCH and SwissTargetPrediction, while endometriosis-related genes were obtained from GeneCards, OMIM, and TTD. Common targets were subjected to PPI network construction and GO/KEGG enrichment analysis. MR analysis was performed to evaluate causality between IL1B expression and endometriosis risk. Molecular docking was used to validate the binding potential of triclosan to key proteins.

Results

A total of 19 overlapping genes were identified between triclosan- and endometriosis-related targets. PPI network analysis revealed IL1B, SRC, EGFR, and KDR as hub genes. Enrichment analysis indicated significant involvement in MAPK signaling, VEGF signaling, and endocrine-related pathways. MR analysis supported a potential causal relationship between IL1B and endometriosis (MR-Egger OR = 2.66, P < 0.05). Docking simulations demonstrated stable binding of triclosan to all four hub targets, with binding energies ranging from − 5.3 to − 5.9 kcal/mol.

Conclusion

This study provides mechanistic insights into the potential role of triclosan in endometriosis development, highlighting IL1B as a possible causal mediator. These findings contribute to a better understanding of environmental risk factors in endometriosis and offer potential molecular targets for future research.