• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

综合生物信息学分析筛选出特发性肺纤维化的关键基因和通路。

Integrated bioinformatics analysis screened the key genes and pathways of idiopathic pulmonary fibrosis.

作者信息

Wu Juan, Wei Yangyang, Kang Hong, Yu Xiao, Wei Shuting, Xue Ting, Kong Xiaomei

机构信息

NHC Key Laboratory of Pneumoconiosis, Shanxi Key Laboratory of Respiratory Diseases, Department of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Taiyuan, China.

出版信息

Sci Rep. 2025 Apr 25;15(1):14448. doi: 10.1038/s41598-025-97037-9.

DOI:10.1038/s41598-025-97037-9
PMID:40280949
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12032202/
Abstract

To investigate the molecular mechanisms underlying idiopathic pulmonary fibrosis (IPF), we analyzed the GSE173355 and GSE173356 datasets obtained from the NCBI-GEO database. We identified differentially expressed genes (DEGs) and differentially methylated sites. Functional enrichment analysis was conducted for both DEGs and differentially methylated sites. Functional enrichment analysis was performed for both DEGs and differentially methylated sites, alongside an examination of immune-related scores, proportions, and GSVA enrichment scores of immune cells in IPF versus control samples. An integrated gene-methylation association analysis revealed 8 genes with expression levels negatively influenced by methylation. The Rap1 pathway, Focal adhesion, and Axon guidance were significantly enriched among both DEGs and differentially methylated sites. Immune-related scores were notably lower in the IPF group compared to the control group, with marked differences in immune cell proportions and GSVA enrichment scores. Screening of DEGs identified 361 differentially expressed immune-related genes (IRGs). Protein-protein interaction (PPI) network analysis using the STRING database and Cytoscape software unveiled 10 key genes and 3 core subnetworks. RT-qPCR validation in bleomycin-induced IPF mouse model and A549 EMT model confirmed the reliability of most findings. These results provide new insights into IPF pathogenesis and potential therapeutic strategies, necessitating further functional validation.

摘要

为了研究特发性肺纤维化（IPF）潜在的分子机制，我们分析了从NCBI - GEO数据库获得的GSE173355和GSE173356数据集。我们鉴定了差异表达基因（DEGs）和差异甲基化位点。对DEGs和差异甲基化位点都进行了功能富集分析。对DEGs和差异甲基化位点进行了功能富集分析，同时检查了IPF与对照样本中免疫相关评分、免疫细胞比例和GSVA富集评分。综合基因 - 甲基化关联分析揭示了8个表达水平受甲基化负面影响的基因。Rap1通路、粘着斑和轴突导向在DEGs和差异甲基化位点中均显著富集。与对照组相比，IPF组的免疫相关评分显著较低，免疫细胞比例和GSVA富集评分存在明显差异。对DEGs的筛选鉴定出361个差异表达的免疫相关基因（IRGs）。使用STRING数据库和Cytoscape软件进行的蛋白质 - 蛋白质相互作用（PPI）网络分析揭示了关键基因和3个核心子网。在博来霉素诱导的IPF小鼠模型和A549上皮 - 间质转化（EMT）模型中进行的RT - qPCR验证证实了大多数研究结果的可靠性。这些结果为IPF发病机制和潜在治疗策略提供了新见解，需要进一步的功能验证。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/8b8bd9368c73/41598_2025_97037_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/f10fe58c9c25/41598_2025_97037_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/edb95114aadd/41598_2025_97037_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/e8a70b8e0793/41598_2025_97037_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/dba00246f16b/41598_2025_97037_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/ed33b4a246b8/41598_2025_97037_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/a272e063db1e/41598_2025_97037_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/e466f1b7692a/41598_2025_97037_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/8b8bd9368c73/41598_2025_97037_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/f10fe58c9c25/41598_2025_97037_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/edb95114aadd/41598_2025_97037_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/e8a70b8e0793/41598_2025_97037_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/dba00246f16b/41598_2025_97037_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/ed33b4a246b8/41598_2025_97037_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/a272e063db1e/41598_2025_97037_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/e466f1b7692a/41598_2025_97037_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00ff/12032202/8b8bd9368c73/41598_2025_97037_Fig8_HTML.jpg

相似文献

1
Integrated bioinformatics analysis screened the key genes and pathways of idiopathic pulmonary fibrosis.综合生物信息学分析筛选出特发性肺纤维化的关键基因和通路。
Sci Rep. 2025 Apr 25;15(1):14448. doi: 10.1038/s41598-025-97037-9.
2
Identification and Validation of Potential Biomarkers and Pathways for Idiopathic Pulmonary Fibrosis by Comprehensive Bioinformatics Analysis.综合生物信息学分析鉴定和验证特发性肺纤维化的潜在生物标志物和途径。
Biomed Res Int. 2021 Jul 4;2021:5545312. doi: 10.1155/2021/5545312. eCollection 2021.
3
Underlying Molecular Mechanism and Construction of a miRNA-Gene Network in Idiopathic Pulmonary Fibrosis by Bioinformatics.生物信息学方法研究特发性肺纤维化中 miRNA-基因网络的潜在分子机制与构建
Int J Mol Sci. 2023 Aug 27;24(17):13305. doi: 10.3390/ijms241713305.
4
Identification and analysis of extracellular matrix and epithelial-mesenchymal transition-related genes in idiopathic pulmonary fibrosis by bioinformatics analysis and experimental validation.通过生物信息学分析和实验验证对特发性肺纤维化中细胞外基质和上皮-间质转化相关基因进行鉴定与分析
Gene. 2025 Jul 10;956:149464. doi: 10.1016/j.gene.2025.149464. Epub 2025 Apr 3.
5
Contribution of cuproptosis and immune-related genes to idiopathic pulmonary fibrosis disease.铜死亡和免疫相关基因在特发性肺纤维化疾病中的作用
Front Immunol. 2025 Feb 7;16:1458341. doi: 10.3389/fimmu.2025.1458341. eCollection 2025.
6
Integrated bioinformatics analysis for the identification of idiopathic pulmonary fibrosis-related genes and potential therapeutic drugs.用于鉴定特发性肺纤维化相关基因和潜在治疗药物的综合生物信息学分析
BMC Pulm Med. 2023 Oct 4;23(1):373. doi: 10.1186/s12890-023-02678-z.
7
Identification of Ferroptosis-Inflammation Related Hub Genes and the Disease Subtypes in Idiopathic Pulmonary Fibrosis via System Biology Approaches.通过系统生物学方法鉴定特发性肺纤维化中与铁死亡-炎症相关的枢纽基因及疾病亚型
Mol Biotechnol. 2025 Apr;67(4):1720-1733. doi: 10.1007/s12033-024-01158-x. Epub 2024 May 11.
8
Identification and Validation of Genes Exhibiting Dynamic Alterations in Response to Bleomycin-Induced Pulmonary Fibrosis.鉴定和验证在博来霉素诱导的肺纤维化反应中表现出动态变化的基因。
Mol Biotechnol. 2024 Nov;66(11):3323-3335. doi: 10.1007/s12033-023-00943-4. Epub 2023 Nov 4.
9
Bioinformatics analysis on differentially expressed genes of alveolar macrophage in IPF.特发性肺纤维化中肺泡巨噬细胞差异表达基因的生物信息学分析
Exp Lung Res. 2019 Nov-Dec;45(9-10):288-296. doi: 10.1080/01902148.2019.1680765. Epub 2019 Nov 24.
10
Construction of an artificial neural network diagnostic model and investigation of immune cell infiltration characteristics for idiopathic pulmonary fibrosis.构建人工神经网络诊断模型并探讨特发性肺纤维化的免疫细胞浸润特征。
BMC Pulm Med. 2024 Sep 17;24(1):458. doi: 10.1186/s12890-024-03249-6.

本文引用的文献

1
Targeting the PI3K/mTOR pathway in idiopathic pulmonary fibrosis: Advances and therapeutic potential.针对特发性肺纤维化中 PI3K/mTOR 通路：进展和治疗潜力。
Bioorg Med Chem. 2024 Dec 1;115:117908. doi: 10.1016/j.bmc.2024.117908. Epub 2024 Sep 5.
2
Association between MAPK and PI3K/Akt signaling pathway-related gene polymorphisms and migraine.MAPK 和 PI3K/Akt 信号通路相关基因多态性与偏头痛的关系。
Mol Genet Genomic Med. 2024 Aug;12(8):e2503. doi: 10.1002/mgg3.2503.
3
Mapping spatially resolved transcriptomes in human and mouse pulmonary fibrosis.
在人和鼠的肺纤维化中定位空间分辨转录组。
Nat Genet. 2024 Aug;56(8):1725-1736. doi: 10.1038/s41588-024-01819-2. Epub 2024 Jul 1.
4
Current state of signaling pathways associated with the pathogenesis of idiopathic pulmonary fibrosis.特发性肺纤维化发病机制相关信号通路的研究现状。
Respir Res. 2024 Jun 17;25(1):245. doi: 10.1186/s12931-024-02878-z.
5
Fibroblast growth factor 21 alleviates idiopathic pulmonary fibrosis by inhibiting PI3K-AKT-mTOR signaling and stimulating autophagy.成纤维细胞生长因子 21 通过抑制 PI3K-AKT-mTOR 信号通路和刺激自噬来减轻特发性肺纤维化。
Int J Biol Macromol. 2024 Jul;273(Pt 1):132896. doi: 10.1016/j.ijbiomac.2024.132896. Epub 2024 Jun 6.
6
Quantitative proteomics identifies tumour matrisome signatures in patients with non-small cell lung cancer.定量蛋白质组学鉴定非小细胞肺癌患者的肿瘤基质组特征。
Front Oncol. 2023 Jun 16;13:1194515. doi: 10.3389/fonc.2023.1194515. eCollection 2023.
7
Idiopathic pulmonary fibrosis.特发性肺纤维化。
Radiologia (Engl Ed). 2022 Dec;64 Suppl 3:227-239. doi: 10.1016/j.rxeng.2022.10.009.
8
DNA methylation: a historical perspective.DNA 甲基化：历史视角。
Trends Genet. 2022 Jul;38(7):676-707. doi: 10.1016/j.tig.2022.03.010. Epub 2022 Apr 30.
9
Axon guidance molecules in immunometabolic diseases.免疫代谢疾病中的轴突导向分子。
Inflamm Regen. 2022 Jan 19;42(1):5. doi: 10.1186/s41232-021-00189-0.
10
Immune dysregulation as a driver of idiopathic pulmonary fibrosis.免疫失调作为特发性肺纤维化的驱动因素。
J Clin Invest. 2021 Jan 19;131(2). doi: 10.1172/JCI143226.