Atherosclerotic plaque instability is a major cause of ischemic stroke. Researchers must develop novel strategies for the detection and treatment of unstable atherosclerotic plaque (UAP)-related stroke. We aimed to identify potential biomarkers and therapeutic targets of UAP-related stroke. Differentially expressed genes (DEGs) of UAP, ischemic stroke and smoking were identified by microarray analyses from the Gene Expression Omnibus. Gene Ontology (GO) and pathway functional enrichment analyses of DEGs were performed to analyze plaque destabilization and ischemic stroke physiopathology. An integrative analysis of UAP, ischemic stroke and smoking DEGs and functional annotations was performed to identify the underlying physiopathology and hub genes in UAP-related stroke and the relationship with smoking. Online search databases were applied to confirm hub gene biofunctions and their relationships with atherosclerosis and cerebrovascular diseases. Following integrative analysis, 18 co-DEGs of UAP and ischemic stroke, including 17 upregulated and one downregulated, were identified. Inflammation, immunity, extracellular matrix degradation, blood coagulation, apoptosis and nerve degeneration were the primary physiopathological processes in UAP-related stroke. Hub genes included MMP9, ITGAM, CCR1, NCF2 and CD163, among which MMP9 and ITGAM were top 10 genes for both UAP and stroke. Smoking may upregulate MMP9, NCF2, C5AR1 and ANPEP to accelerate plaque destabilization and UAP-related stroke. MMP9, ITGAM, CCR1, NCF2, CD163, hsa-miR-3123 and hsa-miR-144-3p are potential diagnostic and prognostic biomarkers of UAP-related stroke. MMP9 and ITGAM are potential therapeutic targets of UAP-related stroke, which will contribute to the development of novel management strategies.

动脉粥样硬化斑块不稳定性是缺血性中风的主要原因。研究人员必须开发检测和治疗不稳定动脉粥样硬化斑块 (UAP) 相关中风的新策略。我们旨在确定 UAP 相关中风的潜在生物标志物和治疗靶点。UAP、缺血性中风和吸烟的差异表达基因 (DEG) 通过基因表达综合分析的微阵列分析确定。对 DEG 进行基因本体论 (GO) 和通路功能富集分析，以分析斑块不稳定和缺血性中风的病理生理学。对 UAP、缺血性中风和吸烟的 DEG 和功能注释进行综合分析，以确定 UAP 相关中风的潜在病理生理学和中枢基因以及与吸烟的关系。应用在线搜索数据库来确认中枢基因的生物功能及其与动脉粥样硬化和脑血管疾病的关系。经过综合分析，确定了 UAP 和缺血性卒中的 18 个 co-DEG，包括 17 个上调和 1 个下调。炎症、免疫、细胞外基质降解、凝血、细胞凋亡和神经变性是 UAP 相关卒中的主要病理生理过程。Hub基因包括MMP9、ITGAM、CCR1、NCF2和CD163，其中MMP9和ITGAM是UAP和中风的前10位基因。吸烟可能会上调 MMP9、NCF2、C5AR1 和 ANPEP，以加速斑块不稳定和 UAP 相关中风。MMP9、ITGAM、CCR1、NCF2、CD163、hsa-miR-3123 和 hsa-miR-144-3p 是 UAP 相关中风的潜在诊断和预后生物标志物。