Article(id=1291704870264918878, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704771212234905, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.17.021, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1717344000000, receivedDateStr=2024-06-03, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896039786, onlineDateStr=2026-08-05, pubDate=1758038400000, pubDateStr=2025-09-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896039786, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896039786, creator=13701087609, updateTime=1785896039786, updator=13701087609, issue=Issue{id=1291704771212234905, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='17', pageStart='2401', pageEnd='2550', issueExtLink='null', onlineDate='null', pubDate='1758038400000', pubDateStr='2025-09-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896016147, creator='13701087609', updateTime=1785896900366, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291708479866164175, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704771212234905, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291708479866164176, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704771212234905, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=2521, endPage=2525, ext={EN=ArticleExt(id=1291704870688543583, articleId=1291704870264918878, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=The potential mechanism of platelet factor 4 in Alzheimer’s disease explored by bioinformatics analysis, columnId=1246531412438966969, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Reader’s Field, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the potential role of platelet factor 4 (PF4) in Alzheimer’s disease (AD) by network pharmacology and bioinformatics analysis.
Methods PubChem and SwissTargetPrediction databases were used to collect PF4 related targets, GeneCards and DisGeNET databases were used to collect AD targets; the protein-protein interaction (PPI) network was constructed by using STRING database to obtain the protein-protein interaction of common genes. Gene ontology (GO) function and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis of common targets were performed using DAVID database. The VascularSingleCells database was used to query the expression of PF4 in mouse cerebrovascular-related cells, and the AlzData database was used to analyze the verification of PF4 in the data set of known AD patients.
Results A total of 102 PF4-related targets, 2 403 AD targets and 51 common targets were obtained. Enrichment analysis showed that the common argets were mainly involved in cancer pathways, neutrophil extracellular trap formation, Interleukin-17 (IL-17) signaling pathway, platelet activation and relaxin signaling pathway. Analysis of cerebrovascular single cell data showed that PF4 was only expressed in microglia. The results of HPA database analysis showed that PF4 was mainly expressed in the cerebral cortex, and a small part was expressed in the amygdala.
Conclusion PF4 may interfere with AD by improving neuronal viability, oxidative stress and reducing inflammatory response through neutrophil extracellular trapping network formation, IL-17 signaling and other pathways.
, authors=Jing NIU
1, 2, Long-tu LI
1, Jia-jia WANG
1, 2, Qian Xiang
1, 2, Zhi-yan LIU
1, authorsList=Jing NIU, Long-tu LI, Jia-jia WANG, Qian Xiang, Zhi-yan LIU, authorCompany=null, correspAuthors=Zhi-yan LIU, 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=1291704871913280353, articleId=1291704870264918878, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=生信分析初步探索血小板因子4在阿尔茨海默病中的潜在作用机制, columnId=1246531414020219657, journalTitle=中国临床药理学杂志, columnName=读者园地, runingTitle=null, highlight=null, articleAbstract=
目的 应用网络药理学和生信分析技术探讨血小板因子4（PF4）在阿尔茨海默中（AD）的潜在作用。
方法 应用PubChem和SwissTargetPrediction数据库收集PF4的相关靶点、GeneCards和DisGeNET数据库收集AD靶点；用STRING数据库获取共同基因的蛋白质间相互作用关系，构建蛋白-蛋白相互作用（PPI）网络；利用DAVID数据库对共有靶点进行基因本体（GO）功能及京都基因与基因组百科全书（KEGG）通路富集分析；利用VascularSingleCells数据库查询PF4在小鼠脑血管相关细胞内表达情况，通过AlzData数据库分析PF4在已知AD患者数据集中的验证。
结果 统计分析后共整理得到PF4相关靶点102个，AD相关靶点2 403个，2者共同靶点51个。富集分析发现共同靶点主要参与癌症中的通路、中性粒细胞胞外诱捕网形成、白细胞介素-17（IL-17）信号通路、血小板活化和松弛素信号通路等；脑血管单细胞数据中分析得到PF4仅在小胶质细胞中表达。HPA数据库分析结果表明PF4在人脑中RNA表达主要在大脑皮质区，少部分在杏仁核中表达。
结论 PF4可能是通过中性粒细胞胞外诱捕网形成、IL-17信号通路改善神经元活力、氧化应激和减轻炎性反应，从而影响AD进展。
, authors=牛镜
1, 2, 李龙图
1, 王佳佳
1, 2, 向倩
1, 2, 刘志艳
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牛镜（2000-），女，硕士研究生，主要从事临床药学方面的工作和研究
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