Yu-yao Ji, Siang Wei, R. Xu, Runda Wu, K. Yao, Y. Zou
{"title":"Bioinformatics analysis identifies potential biomarkers for the prediction and treatment of myocardial infarction","authors":"Yu-yao Ji, Siang Wei, R. Xu, Runda Wu, K. Yao, Y. Zou","doi":"10.4103/2470-7511.312597","DOIUrl":null,"url":null,"abstract":"Objectives: The aim of this study was to identify differentially expressed genes (DEGs) related to myocardial infarction (MI), which may serve as research and therapeutic targets. Methods: MI expression profiles were obtained from the Gene Expression Omnibus (GEO) database. DEGs were screened using GEO2R, and DEGs in multiple datasets were identified using Venn diagrams. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG) pathway enrichment analyses were performed using the Database for Annotation, Visualization, and Integrated Discovery v6.8. A protein-protein interaction (PPI) network was constructed using STRING and Cytoscape 3.7.2. Coexpedia was used for gene coexpression network analysis and functional annotation. Results: We identified 50 DEGs in the four datasets, including 29 with important roles in the PPI network. GO functional enrichment analysis revealed the involvement of DEGs in biological processes such as cytokine activation, peptidase inhibition, and chemokine activation. KEGG analysis revealed enrichment in chemokine signaling and cytokine-cytokine receptor interactions. Gene coexpression network analysis identified nine hub genes involved in the occurrence and development of MI including tissue inhibitor of metalloproteinase 1; CD44 antigen; lysyl oxidase; formyl peptide receptor 2; matrix metallopeptidase 3; formyl peptide receptor 1; serine (or cysteine) peptidase inhibitor, clade E, member 1; prostaglandin-endoperoxide synthase 2; and elastin. Conclusions: The hub genes identified may play important roles in MI-related biological processes and represent potential diagnostic and therapeutic targets. Therefore, this study lays a foundation for further exploration of the molecular mechanisms of MI.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"48 - 55"},"PeriodicalIF":0.0000,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardiology Plus","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/2470-7511.312597","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Objectives: The aim of this study was to identify differentially expressed genes (DEGs) related to myocardial infarction (MI), which may serve as research and therapeutic targets. Methods: MI expression profiles were obtained from the Gene Expression Omnibus (GEO) database. DEGs were screened using GEO2R, and DEGs in multiple datasets were identified using Venn diagrams. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG) pathway enrichment analyses were performed using the Database for Annotation, Visualization, and Integrated Discovery v6.8. A protein-protein interaction (PPI) network was constructed using STRING and Cytoscape 3.7.2. Coexpedia was used for gene coexpression network analysis and functional annotation. Results: We identified 50 DEGs in the four datasets, including 29 with important roles in the PPI network. GO functional enrichment analysis revealed the involvement of DEGs in biological processes such as cytokine activation, peptidase inhibition, and chemokine activation. KEGG analysis revealed enrichment in chemokine signaling and cytokine-cytokine receptor interactions. Gene coexpression network analysis identified nine hub genes involved in the occurrence and development of MI including tissue inhibitor of metalloproteinase 1; CD44 antigen; lysyl oxidase; formyl peptide receptor 2; matrix metallopeptidase 3; formyl peptide receptor 1; serine (or cysteine) peptidase inhibitor, clade E, member 1; prostaglandin-endoperoxide synthase 2; and elastin. Conclusions: The hub genes identified may play important roles in MI-related biological processes and represent potential diagnostic and therapeutic targets. Therefore, this study lays a foundation for further exploration of the molecular mechanisms of MI.
目的:本研究旨在鉴定与心肌梗死(MI)相关的差异表达基因(DEGs),作为研究和治疗靶点。方法:从Gene expression Omnibus (GEO)数据库中获取MI表达谱。使用GEO2R筛选deg,并使用维恩图识别多个数据集中的deg。使用Database for Annotation, Visualization, and Integrated Discovery v6.8进行基因本体(GO)和京都基因与基因组百科全书(KEGG)途径富集分析。利用STRING和Cytoscape 3.7.2构建蛋白-蛋白相互作用(PPI)网络。使用Coexpedia进行基因共表达网络分析和功能标注。结果:我们在四个数据集中确定了50个deg,其中29个在PPI网络中起重要作用。氧化石墨烯功能富集分析显示,deg参与生物过程,如细胞因子激活、肽酶抑制和趋化因子激活。KEGG分析显示趋化因子信号和细胞因子-细胞因子受体相互作用富集。基因共表达网络分析鉴定出包括金属蛋白酶组织抑制剂1在内的9个参与心肌梗死发生发展的枢纽基因;CD44抗原;赖氨酰化氧;甲酰基肽受体2;基质金属肽酶3;甲酰基肽受体1;丝氨酸(或半胱氨酸)肽酶抑制剂,分支E,成员1;前列腺素内过氧化物合成酶2;和弹性蛋白。结论:发现的枢纽基因可能在心肌梗死相关的生物学过程中发挥重要作用,具有潜在的诊断和治疗靶点。因此,本研究为进一步探索心肌梗死的分子机制奠定了基础。