Clinical, cosmetic and investigational dermatology · 2026
Exploring the Toxicological Impact of Bisphenol A on Acne Vulgaris via the PLA2G2A-Arachidonic Acid Pathway.
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Xu Wen, Qian Shutong, Gao Qi, Tao Xiaohua, Xu Danfeng
Аннотация
OBJECTIVE: To investigate the potential molecular mechanisms underlying the contribution of environmental bisphenol A (BPA) exposure to acne pathogenesis, with a specific focus on the PLA2G2A-arachidonic acid pathway.
METHODS: We integrated network toxicology and machine learning to identify common target genes linking BPA exposure and acne. Core genes and key pathways were screened through differential expression, gene enrichment, and feature selection algorithms. The findings were validated in independent datasets and further investigated using immune infiltration analysis, molecular docking, and molecular dynamics simulations.
RESULTS: Three core genes were identified, with PLA2G2A being the central hub. Functional enrichment analysis revealed significant involvement of these targets in arachidonic acid metabolism, PI3K-AKT signaling, and IL-6/JAK-STAT3 pathways. PLA2G2A was upregulated in acne lesions and positively correlated with pro-inflammatory immune cell infiltration. Molecular docking and dynamics simulations indicated stable binding between BPA and PLA2G2A.
CONCLUSION: These findings suggest that BPA exposure may contribute to acne development by targeting PLA2G2A, disrupting arachidonic acid metabolism, and modulating the local inflammatory microenvironment. Crucially, this study highlights the environmental risk of endocrine-disrupting chemicals in dermatology and identifies PLA2G2A as a novel, potential therapeutic target for comprehensive acne management.
METHODS: We integrated network toxicology and machine learning to identify common target genes linking BPA exposure and acne. Core genes and key pathways were screened through differential expression, gene enrichment, and feature selection algorithms. The findings were validated in independent datasets and further investigated using immune infiltration analysis, molecular docking, and molecular dynamics simulations.
RESULTS: Three core genes were identified, with PLA2G2A being the central hub. Functional enrichment analysis revealed significant involvement of these targets in arachidonic acid metabolism, PI3K-AKT signaling, and IL-6/JAK-STAT3 pathways. PLA2G2A was upregulated in acne lesions and positively correlated with pro-inflammatory immune cell infiltration. Molecular docking and dynamics simulations indicated stable binding between BPA and PLA2G2A.
CONCLUSION: These findings suggest that BPA exposure may contribute to acne development by targeting PLA2G2A, disrupting arachidonic acid metabolism, and modulating the local inflammatory microenvironment. Crucially, this study highlights the environmental risk of endocrine-disrupting chemicals in dermatology and identifies PLA2G2A as a novel, potential therapeutic target for comprehensive acne management.