基于蛋白质组学探讨IRF7参与脓毒症急性肾损伤的分子机制。

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

作者信息

Xiang Li, Wanli Ma, Jiannan Song, Zhanfei Hu, Qi Zhou, Haibo Li

机构信息

Department of Anesthesiology, Inner Mongolia Autonomous Region, Chifeng Clinical College of Inner Mongolia Medical University, Chifeng, 024000, China.

Department of Anesthesiology, Municipal Hospital of Chifeng, Inner Mongolia Autonomous Region, Chifeng, 024000, China.

出版信息

Proteome Sci. 2025 Jul 17;23(1):6. doi: 10.1186/s12953-025-00244-5.

DOI:10.1186/s12953-025-00244-5

PMID:40676657

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12273476/

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.

摘要

背景

急性肾损伤是脓毒症的常见并发症，其机制非常复杂。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

通过腹腔注射10mg/kg脂多糖诱导急性肾损伤。采用TMT定量蛋白质组学分析对肾组织进行分析。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）通路富集分析和蛋白质-蛋白质相互作用（PPI）网络分析。

结果

我们获得了530个DEPs。GO分析表明，DEPs的生物学过程主要是应激反应。DEPs的分子功能主要集中在催化活性。DEPs的细胞成分主要位于细胞内和细胞质中。KEGG分析表明，DEPs主要参与代谢途径。鉴定出10个具有相互作用程度的关键蛋白，如Isg15、Irf7、Oasl2、Ifit3、Apob、Oasl、Ube2l6、Ifit2、Ifih1和Ifit1。Irf7在大鼠肾组织中显著上调。