To explore the molecular mechanism of IRF7 involved in acute kidney injury in sepsis based on proteomics.

IF 1.6 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS
Li Xiang, Ma Wanli, Song Jiannan, Hu Zhanfei, Zhou Qi, Li Haibo
{"title":"To explore the molecular mechanism of IRF7 involved in acute kidney injury in sepsis based on proteomics.","authors":"Li Xiang, Ma Wanli, Song Jiannan, Hu Zhanfei, Zhou Qi, Li Haibo","doi":"10.1186/s12953-025-00244-5","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Acute kidney injury is a common complication of sepsis, and its mechanism is very complicated. The purpose of this study was to investigate the mechanism of key differentially expressed proteins and their related signaling pathways in the occurrence and development of acute kidney injury in sepsis through proteomics.</p><p><strong>Methods: </strong>Acute kidney injury was induced by intraperitoneal injection of lipopolysaccharide at 10 mg/kg. Renal tissues were analyzed by TMT quantitative proteomic analysis. Differentially expressed proteins (DEPs) were screened. Gene Ontology (GO) function analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and protein-protein interaction (PPI) network analysis were performed.</p><p><strong>Results: </strong>We obtained 530 DEPs. GO analysis showed that the biological process of DEPs was mainly stress response. The molecular functions of DEPs mainly focus on catalytic activity. The cellular components of DEPs were mainly located in the intracellular and cytoplasm. KEGG analysis showed that DEPs were mainly involved in metabolic pathways. Ten key proteins with interaction degree, such as Isg15, Irf7, Oasl2, Ifit3, Apob, Oasl, Ube2l6, Ifit2, Ifih1 and Ifit1 were identified. Irf7 was significantly up-regulated in rat kidney tissues.</p><p><strong>Conclusion: </strong>The upregulation of Irf7 plays an important role in the mechanism of acute renal injury induced by sepsis.</p>","PeriodicalId":20857,"journal":{"name":"Proteome Science","volume":"23 1","pages":"6"},"PeriodicalIF":1.6000,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12273476/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Proteome Science","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s12953-025-00244-5","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMICAL RESEARCH METHODS","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Acute kidney injury is a common complication of sepsis, and its mechanism is very complicated. The purpose of this study was to investigate the mechanism of key differentially expressed proteins and their related signaling pathways in the occurrence and development of acute kidney injury in sepsis through proteomics.

Methods: Acute kidney injury was induced by intraperitoneal injection of lipopolysaccharide at 10 mg/kg. Renal tissues were analyzed by TMT quantitative proteomic analysis. Differentially expressed proteins (DEPs) were screened. Gene Ontology (GO) function analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and protein-protein interaction (PPI) network analysis were performed.

Results: We obtained 530 DEPs. GO analysis showed that the biological process of DEPs was mainly stress response. The molecular functions of DEPs mainly focus on catalytic activity. The cellular components of DEPs were mainly located in the intracellular and cytoplasm. KEGG analysis showed that DEPs were mainly involved in metabolic pathways. Ten key proteins with interaction degree, such as Isg15, Irf7, Oasl2, Ifit3, Apob, Oasl, Ube2l6, Ifit2, Ifih1 and Ifit1 were identified. Irf7 was significantly up-regulated in rat kidney tissues.

Conclusion: The upregulation of Irf7 plays an important role in the mechanism of acute renal injury induced by sepsis.

基于蛋白质组学研究IRF7参与脓毒症急性肾损伤的分子机制。
背景:急性肾损伤是脓毒症的常见并发症,其发病机制十分复杂。本研究旨在通过蛋白质组学研究脓毒症急性肾损伤发生发展过程中关键差异表达蛋白及其相关信号通路的机制。方法:腹腔注射10 mg/kg脂多糖诱导急性肾损伤。肾组织采用TMT定量蛋白质组学分析。筛选差异表达蛋白(DEPs)。进行基因本体(GO)功能分析、京都基因与基因组百科全书(KEGG)途径富集分析和蛋白-蛋白相互作用(PPI)网络分析。结果:共获得dep 530个。GO分析表明,DEPs的生物过程主要是应激反应。DEPs的分子功能主要集中在催化活性方面。DEPs的细胞成分主要分布在胞内和细胞质中。KEGG分析显示DEPs主要参与代谢途径。鉴定出Isg15、Irf7、Oasl2、Ifit3、Apob、Oasl、ube216、Ifit2、Ifih1、Ifit1等10个具有相互作用程度的关键蛋白。Irf7在大鼠肾组织中显著上调。结论:Irf7表达上调在脓毒症致急性肾损伤机制中起重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Proteome Science
Proteome Science 生物-生化研究方法
CiteScore
2.90
自引率
0.00%
发文量
17
审稿时长
4.5 months
期刊介绍: Proteome Science is an open access journal publishing research in the area of systems studies. Proteome Science considers manuscripts based on all aspects of functional and structural proteomics, genomics, metabolomics, systems analysis and metabiome analysis. It encourages the submissions of studies that use large-scale or systems analysis of biomolecules in a cellular, organismal and/or environmental context. Studies that describe novel biological or clinical insights as well as methods-focused studies that describe novel methods for the large-scale study of any and all biomolecules in cells and tissues, such as mass spectrometry, protein and nucleic acid microarrays, genomics, next-generation sequencing and computational algorithms and methods are all within the scope of Proteome Science, as are electron topography, structural methods, proteogenomics, chemical proteomics, stem cell proteomics, organelle proteomics, plant and microbial proteomics. In spite of its name, Proteome Science considers all aspects of large-scale and systems studies because ultimately any mechanism that results in genomic and metabolomic changes will affect or be affected by the proteome. To reflect this intrinsic relationship of biological systems, Proteome Science will consider all such articles.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信