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多维机械分析揭示了双S诱导的精子生成中断

Lei Xu¹, Bin Huang², Shengliang Gu¹

¹The First School of Clinical Medicine, Yunnan University of Chinese Medicine, Kunming, Yunnan 650500, China.

Reproductive toxicology (Elmsford, N.Y.)

|October 10, 2025

概括

双S (BPS) 暴露可能通过干扰关键丸细胞通路来破坏男性生育能力. 研究人员确定了CTSK,GSTZ1和PDE4D作为BPS诱导的精子生成中断的潜在生物标志物.

科学领域:

生殖毒理学生殖毒理学
环境健康环境健康
计算生物学计算生物学

背景情况:

双S (BPS) 是双A的广泛替代品,引发了人们对全球环境暴露的担忧.
BPS对精子生成障碍 (SD) 的影响及其潜在的分子机制仍然不完全理解.

研究的目的:

为了全面阐明BPS诱导精子生成中断的分子机制.
确定BPS诱导的生殖毒性潜在的诊断生物标志物和治疗点.

主要方法:

采用了多维计算策略,整合了网络毒理学,生物信息学,机器学习,单细胞分析和生物分子建模.
利用113种机器学习算法组合进行系统选.
分析了丸组织特定的共同表达网络和单细胞数据.

主要成果:

BPS通过干扰信号通路 (cAMP,MAPK,VEGF,PI3K-Akt) 破坏精子生成,形成一个协同的毒性网络.
确定了CTSK,GSTZ1和PDE4D作为SD和潜在BPS中心目标的核心诊断生物标志物.
枢纽基因在丸生殖细胞类型中特别表达,并与BPS表现出强烈的结合亲和力.

结论:

这项研究为BPS的生殖毒性风险提供了关键的见解,阐明了它对精子生成的影响.
确定了新的生物标志物 (CTSK,GSTZ1,PDE4D) 和BPS诱导的生殖损害的潜在干预目标.
通过多维机制分析,促进对BPS生殖毒理学的理解.

关键词:

生物分子建模模型双 S 是一种双醇.集成机器学习集成机器学习网络毒理学网络毒理学破坏精子生成的破坏.

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