Article(id=1292126438648476252, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.01.019, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1760889600000, receivedDateStr=2025-10-20, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996549521, onlineDateStr=2026-08-06, pubDate=1768579200000, pubDateStr=2026-01-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996549521, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996549521, creator=13701087609, updateTime=1785996549521, updator=13701087609, issue=Issue{id=1292126377440989952, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='1', pageStart='1', pageEnd='147', issueExtLink='null', onlineDate='null', pubDate='1768579200000', pubDateStr='2026-01-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996534929, creator='13701087609', updateTime=1786014708731, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292202603945947673, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292202603950141978, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=119, endPage=123, ext={EN=ArticleExt(id=1292126439072100957, articleId=1292126438648476252, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of the association between albumin and mitophagy in autosomal dominant polycystic kidney disease based on bioinformatics analysis, columnId=1246531412438966969, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Reader’s Field, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the potential mechanisms and related signaling pathways of mitophagy in the occurrence and development of autosomal dominant polycystic kidney disease (ADPKD) using bioinformatics techniques.
Methods The gene expression omnibus (GEO) dataset GSE7869 was downloaded and processed. Differentially expressed genes (DEGs) were identified using the R limma package. Mitophagy-related genes were retrieved from the GeneCards database and intersected with the DEGs to obtain candidate genes. A protein-protein interaction (PPI) network was constructed using STRING, and core genes were identified in Cytoscape using the maximalclique centrality (MCC) algorithm. Gene set enrichment analysis (GSEA) was conducted based on albumin (ALB) expression levels, and R packages including clusterProfiler, ggplot2 and enrichplot were used to visualize and interpret the enrichment results.
Results A total of 248 DEGs were obtained, including 61 up-regulated and 187 down-regulated genes. After intersecting with mitophagy-related genes, 38 candidate DEGs were identified. ALB was identified as the core differentially expressed gene through PPI analysis and Cytoscape. GSEA results indicated that the mitophagy-related gene ALB may play a role in ADPKD by regulating pathways such as extracellular matrix (ECM)-receptor interaction and branched-chain amino acid (BCAA) metabolism, as well as biological processes including organic acid and amino acid metabolism and organization of collagen fibrils.
Conclusions ALB expression levels were significantly associated with pathways including ECM-receptor interaction and branched-chain amino acid metabolism, as well as with biological processes such as organic acid and amino acid metabolism and organization of collagen fibrils. These findings suggest that ALB may be involved in the pathogenesis of ADPKD.
, authors=Sen-tao PAN
1, 2, Zhi-wei QIU
2, Yu CHEN
1, 2, Qian XIANG
2, Yi-min CUI
1, 2, authorsList=Sen-tao PAN, Zhi-wei QIU, Yu CHEN, Qian XIANG, Yi-min CUI, authorCompany=null, correspAuthors=Yi-min CUI, 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=1292126439478948446, articleId=1292126438648476252, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=基于生物信息学探索白蛋白与常染色体显性多囊肾病线粒体自噬机制的相关性研究, 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探讨线粒体自噬在常染色体显性多囊肾病（ADPKD）发生发展中的可能机制及相关信号通路。
方法 下载并处理基因表达数据库（GEO）数据集GSE7869，用R语言“limma”包筛选差异表达基因。在Genecard数据库中检索线粒体自噬相关基因并与差异基因取交集以获得候选基因；用STRING构建蛋白质互作（PPI）网络并在Cytoscape中以最大集团中心度（MCC）算法筛选核心基因；基于白蛋白（ALB）表达水平进行基因集富集分析（GSEA），并用“clusterProfiler”“ggplot2”“enrichplot”等R语言包对富集结果进行可视化与解释。
结果 通过生物信息学分析方法，共获得248个差异基因，包括61个上调基因和187个下调基因。取交集后获得38个与线粒体自噬相关差异基因。通过PPI分析和Cytoscape处理获得核心差异基因ALB。GSEA分析显示，线粒体自噬相关基因ALB可能通过调控细胞外基质（ECM）-受体相互作用、支链氨基酸代谢（BCAA）等途径以及有机酸和氨基酸代谢、胶原纤维组织化等生物过程在常染色体显性多囊肾病中发挥作用。
结论 ALB的表达水平与细胞外基质-受体相互作用、支链氨基酸代谢等途径以及有机酸和氨基酸代谢、胶原纤维组织化等生物过程显著相关，提示其可能参与ADPKD的发生发展。
, authors=潘森涛
1, 2, 邱志维
2, 陈瑜
1, 2, 向倩
2, 崔一民
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潘森涛（2002-），男，硕士研究生，主要从事临床药学方面的相关研究
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