首页|基于生物信息学分析的系统性硬化症合并肺动脉高压靶基因预测

基于生物信息学分析的系统性硬化症合并肺动脉高压靶基因预测

Prediction of target genes for systemic sclerosis-related pulmonary arterial hypertension based on bioinformatical analysis

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目的:用生物信息学方法筛选系统性硬化症合并肺动脉高压的关键基因与信号通路.方法:从GEO数据库下载芯片基因集,用R软件筛选出表达上调的差异基因并导入DAVID和STRING数据库进行GO功能注释和KEGG信号通路富集分析,Cytoscape软件构建蛋白互作网络并筛选关键基因蛋白.用GSEA探索与系统性硬化症合并肺动脉高压相关的KEGG通路及核心基因.结果:共筛选出15个关键基因蛋白,并与NCBI、OMIM、GeneCards中已报道的基因取交集,得到关键基因TLR4和TNFSF10.GSEA分析分别得到两个芯片的247个和274个核心基因,筛选得到核心基因CTSG、PLAUR和FCGR2A.结论:TLR4、TNFSF10、CTSG、PLAUR、FCG2R可能与系统性硬化症合并肺动脉高压的发生发展密切相关,有望成为系统性硬化症合并肺动脉高压早期诊断和精准治疗的潜在靶点.
Objective:To screen the key genes and signaling pathways in systemic sclerosis-related pulmo-nary arterial hypertension using bioinformatics methods.Methods:The microarray gene sets were downloaded from the GEO database,and the up-regulated differential genes were screened by R soft-ware and imported into DAVID and STRING databases for gene ontology(GO)functional annota-tion and KEGG signal pathway enrichment analysis.Cytoscape software was used to construct a pro-tein interaction network and screen key gene proteins.GSEA was used to explore the KEGG pathway and core genes associated with systemic sclerosis-related pulmonary arterial hypertension.Results:A total of 15 key gene proteins were screened out,and the key genes TLR4 and TNFSF10 were ob-tained by intersections with the genes reported in NCBI,OMIM,and GeneCards.There were 247 and 274 core genes of the two microarrays obtained from GSEA analysis,respectively,and core genes CTSG,PLAUR,and FCGR2A were screened.Conclusion:TLR4,TNFSF10,CTSG,PLAUR,and FCG2R may be closely related to the occurrence and development of systemic sclerosis-related pulmonary arterial hypertension and are expected to become potential targets for its early diag-nosis and precise treatment.

Systemic SclerosisPulmonary Arterial HypertensionBioinformaticsGEO Data-baseGSEA

朱太文、王伟

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武汉大学中南医院呼吸与危重症医学科 湖北 武汉 430071

系统性硬化症 肺动脉高压 生物信息学 GEO数据库 GSEA

国家自然科学基金面上项目

81670021

2024

武汉大学学报(医学版)
武汉大学

武汉大学学报(医学版)

CSTPCD
影响因子:0.959
ISSN:1671-8852
年,卷(期):2024.45(1)
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