Article(id=1291705368921534638, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404807152067353, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.08.022, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1731081600000, receivedDateStr=2024-11-09, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896158675, onlineDateStr=2026-08-05, pubDate=1745769600000, pubDateStr=2025-04-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896158675, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896158675, creator=13701087609, updateTime=1785896158675, updator=13701087609, issue=Issue{id=1291404807152067353, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='8', pageStart='1051', pageEnd='1200', issueExtLink='null', onlineDate='null', pubDate='1745769600000', pubDateStr='2025-04-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824499166, creator='13701087609', updateTime=1785897109470, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291709356903522905, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404807152067353, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291709356903522906, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404807152067353, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1175, endPage=1179, ext={EN=ArticleExt(id=1291705369110278319, articleId=1291705368921534638, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Exploration the mechanism of ATF3 participating in cell senescence of hypertensive nephropathy based on bioinformatics analysis, columnId=1246531412438966969, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Reader’s Field, runingTitle=null, highlight=null, articleAbstract=
Objective To study the possible mechanism and related signaling pathway of cell senescence in hypertensive nephropathy with the help of bioinformatics.
Methods The microarray data GSE37455 was downloaded from the gene expression database, and the data was merged with R software to remove the batch effect, so as to obtain differentially expressed genes. Cell aging genes were obtained from the CellAge database, and differential genes related to cell aging were obtained through R package “ggVennDiagram”. Gene interaction network string database was imported to obtain protein protein interaction (PPI) network map, and Cytoscape3.8.0 software was used to mine core differential genes. The function and pathway of core differential genes were analyzed by gene ontology (GO), Kyoto encyclopedia of genes and genomes (KEGG) and gene set enrichment analysis (GSEA).
Results A total of 41 differential genes were obtained, including 32 up-regulated genes and 9 down-regulated genes. Four differential genes related to cell senescence were obtained after intersection. The core differential gene-activated transcription factor 3(ATF3) was obtained by PPI analysis and Cytoscape treatment. GSEA analysis showed that cell senescence might play a role in hypertensive nephropathy through the thermogenesis of mitochondrial uncoupling protein 1 and the signal transduction of type Ⅰ interferon response (TYPE-Ⅰ-IFN).
Conclusion Cellular senescence may play a role in hypertensive nephropathy through pathways such as mitochondrial uncoupling protein-1 thermogenesis and TYPE-Ⅰ-IFN signaling, which provides a therapeutic target for the study of hypertensive nephropathy.
, authors=Yu CHEN
1, 2, Zhi-wei QIU
2, Xin LUO
1, 2, Jia-jia WANG
2, 3, Qian XIANG
1, 2, authorsList=Yu CHEN, Zhi-wei QIU, Xin LUO, Jia-jia WANG, Qian XIANG, authorCompany=null, correspAuthors=Qian XIANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291705370913829040, articleId=1291705368921534638, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=基于生物信息学探索ATF3参与高血压肾病细胞衰老的相关机制, columnId=1246531414020219657, journalTitle=中国临床药理学杂志, columnName=读者园地, runingTitle=null, highlight=null, articleAbstract=
目的 借助生物信息学技术研究细胞衰老在高血压肾病中可能发生的机制及相关信号通路。
方法 查找基因表达数据库下载微阵列数据GSE37455，用R软件合并数据并去除批次效应，获取差异表达基因。从细胞衰老基因CellAge数据库获取细胞衰老基因，通过R包“ggVennDiagram”获取与细胞衰老相关差异基因。导入基因相互作用网络String数据库获取蛋白质互作（PPI）网络图，用Cytoscape 3.8.0软件挖掘核心差异基因。用基因本体（GO）、京都基因与基因组百科全书（KEGG）、基因集富集分析（GSEA）对核心差异基因进行功能和通路分析。
结果 共获得41个差异基因，包括32个上调基因和9个下调基因。取交集后获得4个与细胞衰老相关差异基因。通过PPI分析和Cytoscape处理获得核心差异基因激活转录因子3（ATF3）。GSEA分析显示，细胞衰老可能通过线粒体解偶联蛋白1产热、Ⅰ型干扰素反应（TYPE-Ⅰ-IFN）的信号传导等途径在高血压肾病中发挥作用。
结论 细胞衰老在高血压肾病中可能通过线粒体解偶联蛋白1产热、TYPE-Ⅰ-IFN等途径发生作用，为高血压肾病的研究提供治疗靶点。
, authors=陈瑜
1, 2, 邱志维
2, 罗鑫
1, 2, 王佳佳
2, 3, 向倩
1, 2, authorsList=陈瑜, 邱志维, 罗鑫, 王佳佳, 向倩, authorCompany=null, correspAuthors=向倩, authorNote=
陈瑜（2002-），女，硕士研究生，主要从事临床药学方面的相关研究
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1.School of Pharmacy, Wenzhou Medical University, Wenzhou 325035, Zhejiang Province, China
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1.温州医科大学 药学院，浙江 温州 325035
2.北京大学 第一医院 临床药理研究所，北京 100034, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null)}, companyList=[AuthorCompany(id=1291705371287122097, tenantId=1146029695717560320, journalId=1246415772164075586, articleId=1291705368921534638, xref=1., ext=[AuthorCompanyExt(id=1291705371295510706, tenantId=1146029695717560320, journalId=1246415772164075586, articleId=1291705368921534638, companyId=1291705371287122097, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=
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2.Institute of Clinical Pharmacology, Peking University First Hospital, Beijing 100034, China
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2.北京大学 第一医院 临床药理研究所，北京 100034
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1, 2, address=
1.School of Pharmacy, Wenzhou Medical University, Wenzhou 325035, Zhejiang Province, China
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1.温州医科大学 药学院，浙江 温州 325035
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