鉴定与甲相关的毒理目标及其在慢性阻塞性肺病病原体中的作用:全面的生物信息学和机器学习方法

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Jiehua Deng¹, Lixia Wei^2,3, Yongyu Chen⁴

¹Department of Respiratory and Critical Medicine, The Eighth Affiliated Hospital, Sun Yat-sen University, 3025 Shennan Zhong Lu, Shenzhen City, Guangdong Province, 518033, China.

BMC pharmacology & toxicology

|February 18, 2025

概括

甲 (BaP) 暴露有助于慢性阻塞性肺病 (COPD). 这项研究确定了关键的毒理标,揭示了氧化应激和炎症途径驱动免疫细胞透,为BaP诱导的COPD提供了潜在的生物标志物和治疗标.

科学领域:

环境毒理学环境毒理学
肺部医学肺部医学
生物信息学是一种生物信息学.

背景情况:

环境因素,如甲 (BaP) 暴露,显著影响慢性阻塞性肺病 (COPD) 病原体.
了解BaP诱导的COPD的具体毒理目标和分子机制对于开发有效干预措施至关重要.

研究的目的:

在慢性阻塞性肺病 (COPD) 的背景下,确定与子甲烯 (BaP) 暴露相关的毒理目标.
为了阐明分子途径和免疫细胞参与BaP诱导的COPD.
开发一种用于对暴露于BaP的个体进行COPD风险评估的预测模型.

主要方法:

一种综合生物信息学方法,集成数据库 (CTD,超级PRED),基因表达数据 (GSE76925) 和蛋白质与蛋白质相互作用网络.
进行了功能丰富 (GO,KEGG) 和免疫透 (ssGSEA) 分析.
机器学习算法 (SVM-RFE,Lasso,RF) 识别了特征基因,随后进行了名字结构和分子对接.

主要成果:

在COPD中确定了72个差异表达的BaP相关标,其中的途径与氧化应激和炎症有关.
显著的免疫细胞透 (B细胞,巨细胞,T细胞等). 在COPD患者中观察到.
鉴定了七个特征基因 (ACE,APOE,CDK1,CTNNB1,GATA6,IRF1,SLC1A3),一个名图显示出高的诊断准确性. BaP与CDK1.1具有很高的结合亲和力.

结论:

暴露于BaP会通过氧化应激和炎症促进COPD,导致免疫细胞透.
已识别的特征基因代表了BaP诱导的COPD的潜在生物标志物和治疗点.
开发的诺米图为预测暴露人群中COPD风险提供了有价值的临床工具.

关键词:

子甲烯 (a) 甲烯生物信息学是一种生物信息学.慢性阻塞性肺病是一种慢性阻塞性肺病.免疫评分免疫评分免疫评分凯格 (KEGG) 是一个多环芳香碳化合物多环芳香碳化合物

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