目的 基于生物信息学视角探索糖尿病(diabetes mellitus,DM)和动脉粥样硬化(atherosclerosis,AS)的共病机制.方法 通过分析GEO数据库中DM和AS基因表达谱,筛选差异表达基因(differentially expressed gene,DEG)并进行基因本体(gene ontology,GO)和京都基因与基因组百科全书(Kyoto encyclopedia of genes and genomes,KEGG)富集分析.利用 CytoScape 软件构建DEG的蛋白互作网络并筛选核心基因.富集分析核心基因的生物学功能.结果 本研究共鉴定出77个重叠的DEG.富集分析结果显示,这些DEG主要涉及免疫响应、细胞内外部结构以及免疫相关活性的调控等多个生物学通路.筛选出15个核心基因.GO和KEGG富集分析结果显示,它们在调节免疫反应、参与炎性信号转导、调控代谢通路等过程中发挥关键作用.与吞噬体、中性粒细胞胞外陷阱形成、Toll样受体信号通路、脂质和AS等多个通路密切相关.结论 DM和AS共病机制主要涉及炎症和免疫反应等方面,核心基因在调节免疫反应、参与炎性信号转导、调控代谢通路等过程中发挥关键作用.
Exploring the Comorbidity Mechanisms of Diabetes Mellitus and Atherosclerosis from the Bioinformatics Perspective
Objective To investigate the comorbidity mechanisms between diabetes mellitus(DM)and atherosclerosis(AS)from the perspective of bioinformatics.Methods By analyzing gene expression profiles of DM and AS from the GEO database,differentially expressed gene(DEG)were identified and subjected to enrichment analysis.The CytoScape software was utilized to construct a protein-protein interaction network of DEG and to select core genes.Gene ontology(GO)and Kyoto encyclopedia of genes and genomes(KEGG)enrichment analysis was performed to elucidate the biological functions of the core genes.Results A total of 77 overlapping DEG were i-dentified.Enrichment analysis showed that these DEG were mainly involved in multiple biological pathways including immune response,intracellular and extracellular structure,and regulation of immune-related activities.Fifteen core genes were selected,and GO and KEGG enrichment analysis revealed their critical roles in regulating immune responses,participating in inflammation signaling pathways,and regulating metabolic pathways.They were closely related to multiple pathways including phagosome,formation of neutrophil extracel-lular traps,Toll-like receptor signaling pathways,lipid and AS.Conclusion The common pathogenesis mechanisms of DM and AS pri-marily involve inflammation and immune responses.Core genes play a crucial role in regulating immune responses,participating in inflam-matory signal transduction,and modulating metabolic pathways.
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