基于生物信息学寻找原发性干燥综合征继发颈动脉硬化的潜在机制

Finding the Underlying Mechanism of Carotid Atherosclerosis in Primary Sjogren's Syndrome Based on Bioinformatics

目的:挖掘干燥综合征发生颈动脉硬化的关键信号分子,为进一步阐明干燥综合征发生颈动脉硬化提供生物信息学基础。方法:利用GEO数据库,数据来源于两个芯片,分别是颈动脉硬化经内膜剥脱后的标本芯片GSE12128和原发性干燥综合征的多组学芯片GSE84844。GEO2R工具用于筛选两组基因芯片的差异表达基因。采用在线分析网站Daivid数据库进行GEO和Pathway分析。利用Cytoscape对获得的差异基因数据进行可视化,并利用Cytohubbe筛选核心基因。结果:共鉴定出372个下调基因,选出10个连接度较高的核心基因。发现G蛋白耦联受体活化通路、多巴胺能突触以及神经活性受体-配体活化。结论:GNGT1的过度表达可能是干燥综合征发生颈动脉硬化的潜在机制,其发生的通路与G蛋白耦联受体活化通路、多巴胺能突触以及神经活性受体-配体活化等有关。

Objective To uncover key signaling molecules that contribute to the occurrence of carotid artery atherosclerosis in Sjögren syndrome,providing a bioinformatics foundation for a deeper understanding of the pathological process.Method We utilized the GEO database,employing data from carotid artery atherosclerosis specimens(GSE12128)and primary Sjögren syndrome multiomics chips(GSE84844).Differential expression genes between the two sets of gene chips were screened using the GEO2R tool,and GEO and pathway analyses were conducted using the Daivid database.The differential gene data were visualized using Cytoscape,and core genes were selected using cytohubbe.Results A total of 372 downregulated genes were revealed,with 10 core genes identified based on high connectivity.We found G protein-coupled receptor activation pathways,dopaminergic synapses,and neuroactive receptor-ligand activation.Conclusion Among them,the overexpression of GNGT1 may represent a potential mechanism for the occurrence of carotid artery atherosclerosis in Sjögren syndrome,with pathways associated with G protein-coupled receptor activation,dopamine synapses,and neuroactive receptor-ligand activation.