The current research aimed to expound the genes and pathways that are involved in coronary artery disease (CAD) and ischaemic stroke (IS) and the related mechanisms. Two array CAD datasets of (GSE66360 and GSE97320) and an array IS dataset (GSE22255) were downloaded. Differentially expressed genes (DEGs) were identified using the limma package. The online tool Database for Annotation, Visualization and Integrated Discovery (DAVID) (version 6.8; david.abcc.ncifcrf.gov) was used to annotate the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) enrichment analyses of the DEGs. A protein-protein interaction (PPI) network was constructed by Cytoscape software, and then Molecular Complex Detection (MCODE) analysis was used to screen for hub genes. The hub genes were also confirmed by RT-qPCR and unconditional logistic regression analysis in our CAD and IS patients. A total of 20 common DEGs (all upregulated) were identified between the CAD/IS and control groups. Eleven molecular functions, 3 cellular components, and 49 biological processes were confirmed by GO enrichment analysis, and the 20 common upregulated DEGs were enriched in 21 KEGG pathways. A PPI network including 24 nodes and 68 edges was constructed with the STRING online tool. After MCODE analysis, the top 5 high degree genes, including Jun proto-oncogene (JUN, degree = 9), C-X-C motif chemokine ligand 8 (CXCL8, degree = 9), tumour necrosis factor (TNF, degree = 9), suppressor of cytokine signalling 3 (SOCS3, degree = 8) and TNF alpha induced protein 3 (TNFAIP3, degree = 8) were noted. RT-qPCR results demonstrated that the expression levels of CXCL8 were increased in IS patients than in normal participants and the expression levels of SOCS3, TNF and TNFAIP were higher in CAD/IS patients than in normal participants. Meanwhile, unconditional logistic regression analysis revealed that the incidence of CAD or IS was positively correlated with the CXCL8, SOCS3, TNF and TNFAIP3. The CXCL8, TNF, SOCS3 and TNFAIP3 associated with inflammation may serve as biomarkers for the diagnosis of CAD or IS. The possible mechanisms may involve the Toll-like receptor, TNF, NF-kappa B, cytokine-cytokine receptor interactions and the NOD-like receptor signalling pathways.

中文翻译：

---

与炎症相关的基因可以作为诊断冠状动脉疾病和缺血性中风的生物标志物

目前的研究旨在阐明涉及冠状动脉疾病（CAD）和缺血性中风（IS）的基因和途径及其相关机制。下载了两个阵列CAD数据集（GSE66360和GSE97320）和一个阵列IS数据集（GSE22255）。使用limma软件包识别差异表达基因（DEG）。用于注释，可视化和集成发现的在线工具数据库（DAVID）（版本6.8； david.abcc.ncifcrf.gov）用于注释《京都议定书》中的基因和基因组百科全书（KEGG）途径以及基因本体论（GO）富集分析DEG。通过Cytoscape软件构建了蛋白质-蛋白质相互作用（PPI）网络，然后使用分子复合物检测（MCODE）分析来筛选集线器基因。还通过RT-qPCR和无条件logistic回归分析在我们的CAD和IS患者中证实了枢纽基因。在CAD / IS和对照组之间总共确定了20个常见的DEG（均被上调）。GO富集分析确认了11种分子功能，3个细胞成分和49个生物学过程，而20种常见上调的DEGs在21条KEGG途径中富集了。使用STRING在线工具构建了一个包含24个节点和68个边的PPI网络。经过MCODE分析后，前5个高度基因包括Jun原癌基因（JUN​​，度= 9），CXC基序趋化因子配体8（CXCL8，度= 9），肿瘤坏死因子（TNF，度= 9），抑制因子注意到细胞因子信号传导3（SOCS3，度= 8）和TNFα诱导蛋白3（TNFAIP3，度= 8）。RT-qPCR结果表明，IS患者中CXCL8的表达水平高于正常参与者，而CAD / IS患者中SOCS3，TNF和TNFAIP的表达水平高于正常参与者。同时，无条件logistic回归分析显示，CAD或IS的发生与CXCL8，SOCS3，TNF和TNFAIP3正相关。与炎症相关的CXCL8，TNF，SOCS3和TNFAIP3可用作诊断CAD或IS的生物标志物。可能的机制可能涉及Toll样受体，TNF，NF-κB，细胞因子-细胞因子受体相互作用和NOD样受体信号通路。CAD / IS患者的TNF和TNFAIP高于正常参与者。同时，无条件logistic回归分析显示，CAD或IS的发生与CXCL8，SOCS3，TNF和TNFAIP3正相关。与炎症相关的CXCL8，TNF，SOCS3和TNFAIP3可以作为诊断CAD或IS的生物标志物。可能的机制可能涉及Toll样受体，TNF，NF-κB，细胞因子-细胞因子受体相互作用和NOD样受体信号通路。CAD / IS患者的TNF和TNFAIP高于正常参与者。同时，无条件logistic回归分析显示，CAD或IS的发生与CXCL8，SOCS3，TNF和TNFAIP3正相关。与炎症相关的CXCL8，TNF，SOCS3和TNFAIP3可以作为诊断CAD或IS的生物标志物。可能的机制可能涉及Toll样受体，TNF，NF-κB，细胞因子-细胞因子受体相互作用和NOD样受体信号通路。