环境触发因素和未来发展自身免疫性疾病的风险:双A分子机制和网络毒理学分析

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Yanggang Hong¹, Deqi Wang², Yinfang Lin²

¹The Second School of Medicine, Wenzhou Medical University, Zhejiang Province 325035, China.

Ecotoxicology and environmental safety

|November 17, 2024

概括

双甲 (BPA) 暴露可能通过影响免疫功能引发自身免疫性疾病 (ADs). 这项研究确定了关键的分子标,将BPA与类风湿性关节炎和狼等疾病联系起来,突出了环境风险因素.

科学领域:

环境毒理学环境毒理学
免疫学免疫学免疫学
计算生物学计算生物学

背景情况:

双A (BPA) 是塑料中常见的化学物质,与有害健康影响有关.
暴露于BPA与免疫功能障碍和自身免疫性疾病 (ADS) 的发展有关.
通过BPA诱导AD的确切机制在很大程度上是未知的.

研究的目的:

通过网络毒理学研究BPA诱导的自身免疫的分子机制.
确定BPA在ADS中的作用中涉及的潜在分子标和途径.
探索BPA作为各种自身免疫性疾病的环境触发因素.

主要方法:

使用数据库 (ChEMBL,STITCH,SwissTargetPrediction,GeneCards,OMIM) 来识别与BPA和AD相关的目标.
使用STRING和Cytoscape进行网络分析,以确定核心目标.
通过Metascape进行丰富分析和来自GEO数据库的基因表达分析.
与Autodock进行分子对接,以确认BPA与关键目标的结合.

主要成果:

确定了包括PPARG,CTNNB1,ESR1,EGFR,SRC和CCND1在内的核心目标,这些目标在ADs中表现出改变.
证实了BPA与这些核心目标之间强烈的绑定亲和力.
在多个ADS中揭示了已识别的目标的显著上调或下调.

结论:

暴露于BPA是一种潜在的环境因素,有助于自身免疫性疾病的发展.
这项研究阐明了BPA可能引发自身免疫的潜在分子通路.
这些发现强调了对自身免疫性疾病环境风险评估的重要性.

关键词:

自身免疫性疾病是一种自身免疫性疾病.双 A 是一种双.环境暴露环境暴露环境暴露分子对接是分子对接.网络毒理学网络毒理学

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