• 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

激素性股骨头坏死患者的差异基因表达和免疫细胞浸润。

Differential Gene Expression and Immune Cell Infiltration in Patients with Steroid-induced Necrosis of the Femoral Head.

机构信息

Guangxi University of Traditional Chinese Medicine, Nanning City, Guangxi Zhuang Autonomous Region, 530001, China.

Department of Orthopedics, Wenshan Prefecture Traditional Chinese Medicine Hospital, Yun Nan Region, 663100 China.

出版信息

Endocr Metab Immune Disord Drug Targets. 2024;24(12):1377-1394. doi: 10.2174/0118715303266951231206114153.

DOI:10.2174/0118715303266951231206114153
PMID:38204239
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11348512/
Abstract

OBJECTIVE

The study aimed to study the differential gene expression and immune cell infiltration in patients with steroid-induced necrosis of the femoral head (SANFH), identify the key genes and immune cells of SANFH, and explore the relationship between immune cells and SANFH.

METHODS

The high-throughput gene chip dataset GSE123568 was downloaded from the GEO database, and the differential gene expression was analyzed with the R language. The STRING database and Cytoscape software were used to analyze the protein interaction network and screen key genes, and enrichment analysis was carried out on key genes. The infiltration of immune cells in SANFH patients was analyzed and verified by immunohistochemistry.

RESULTS

EP300, TRAF6, STAT1, JAK1, CASP8, and JAK2 are key genes in the pathogenesis of SANFH, which mainly involve myeloid cell differentiation, cytokine-mediated signaling pathway, tumor necrosis factor-mediated signaling pathway, and cellular response to tumor necrosis factor through JAK-STAT, NOD-like receptor, toll-like receptor, and other signaling pathways, leading to the occurrence of diseases; immune infiltration and immunohistochemical results have shown the expression of memory B cells and activated dendritic cells as reduced in SANFH patients, while in the same SANFH samples, M1 macrophages have been positively correlated with monocytes, and neutrophils have been negatively correlated with monocytes expression.

CONCLUSION

EP300, TRAF6, STAT1, JAK1, CASP8, and JAK2 have exhibited significant differences in SANFH (spontaneous osteonecrosis of the femoral head). Memory B cells, activated dendritic cells, M1 macrophages, monocytes, and neutrophils have shown abnormal expression in SANFH.

摘要

目的

研究激素性股骨头坏死（SANFH）患者的差异基因表达和免疫细胞浸润，鉴定 SANFH 的关键基因和免疫细胞，探讨免疫细胞与 SANFH 的关系。

方法

从 GEO 数据库中下载高通量基因芯片数据集 GSE123568，用 R 语言分析差异基因表达。利用 STRING 数据库和 Cytoscape 软件分析蛋白质互作网络，筛选关键基因，并对关键基因进行富集分析。通过免疫组化分析和验证 SANFH 患者免疫细胞的浸润。

结果

EP300、TRAF6、STAT1、JAK1、CASP8 和 JAK2 是 SANFH 发病机制中的关键基因，主要涉及髓样细胞分化、细胞因子介导的信号通路、肿瘤坏死因子介导的信号通路以及通过 JAK-STAT、NOD 样受体、Toll 样受体等信号通路的细胞对肿瘤坏死因子的反应，导致疾病发生；免疫浸润和免疫组化结果表明，SANFH 患者记忆 B 细胞和活化树突状细胞的表达减少，而在相同的 SANFH 样本中，M1 巨噬细胞与单核细胞呈正相关，中性粒细胞与单核细胞表达呈负相关。

结论

EP300、TRAF6、STAT1、JAK1、CASP8 和 JAK2 在 SANFH（自发性股骨头坏死）中表现出显著差异。记忆 B 细胞、活化树突状细胞、M1 巨噬细胞、单核细胞和中性粒细胞在 SANFH 中表现出异常表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/a3c046d955be/EMIDDT-24-1377_F17.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/085a1ebf248d/EMIDDT-24-1377_F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/e1e7d6ec8c4b/EMIDDT-24-1377_F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/0a2e195b4e4b/EMIDDT-24-1377_F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/dcbe3b7b99ab/EMIDDT-24-1377_F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/c46c296f831a/EMIDDT-24-1377_F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/492a1105172e/EMIDDT-24-1377_F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/0a66d3cc5646/EMIDDT-24-1377_F7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/f48165d06107/EMIDDT-24-1377_F8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/3cbf0527ab04/EMIDDT-24-1377_F9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/17a742d227fb/EMIDDT-24-1377_F10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/dac3b1bf82fa/EMIDDT-24-1377_F11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/8adb87bc92ba/EMIDDT-24-1377_F12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/72da1fe7b50e/EMIDDT-24-1377_F13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/b043ba430159/EMIDDT-24-1377_F14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/60796ae827cc/EMIDDT-24-1377_F15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/2b067b1215bd/EMIDDT-24-1377_F16.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/a3c046d955be/EMIDDT-24-1377_F17.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/085a1ebf248d/EMIDDT-24-1377_F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/e1e7d6ec8c4b/EMIDDT-24-1377_F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/0a2e195b4e4b/EMIDDT-24-1377_F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/dcbe3b7b99ab/EMIDDT-24-1377_F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/c46c296f831a/EMIDDT-24-1377_F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/492a1105172e/EMIDDT-24-1377_F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/0a66d3cc5646/EMIDDT-24-1377_F7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/f48165d06107/EMIDDT-24-1377_F8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/3cbf0527ab04/EMIDDT-24-1377_F9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/17a742d227fb/EMIDDT-24-1377_F10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/dac3b1bf82fa/EMIDDT-24-1377_F11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/8adb87bc92ba/EMIDDT-24-1377_F12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/72da1fe7b50e/EMIDDT-24-1377_F13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/b043ba430159/EMIDDT-24-1377_F14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/60796ae827cc/EMIDDT-24-1377_F15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/2b067b1215bd/EMIDDT-24-1377_F16.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa79/11348512/a3c046d955be/EMIDDT-24-1377_F17.jpg

相似文献

1
Differential Gene Expression and Immune Cell Infiltration in Patients with Steroid-induced Necrosis of the Femoral Head.激素性股骨头坏死患者的差异基因表达和免疫细胞浸润。
Endocr Metab Immune Disord Drug Targets. 2024;24(12):1377-1394. doi: 10.2174/0118715303266951231206114153.
2
Identification of steroid-induced osteonecrosis of the femoral head biomarkers based on immunization and animal experiments.基于免疫和动物实验鉴定激素诱导性股骨头坏死的生物标志物。
BMC Musculoskelet Disord. 2024 Jul 29;25(1):596. doi: 10.1186/s12891-024-07707-4.
3
Network-Based Pharmacology and Bioinformatics Study on the Mechanism of Action of Gujiansan in the Treatment of Steroid-Induced Avascular Necrosis of the Femoral Head.基于网络的药理学和生物信息学研究骨健散治疗激素性股骨头坏死作用机制
Biomed Res Int. 2022 Jul 23;2022:8080679. doi: 10.1155/2022/8080679. eCollection 2022.
4
Identification and analysis of mitochondria-related central genes in steroid-induced osteonecrosis of the femoral head, along with drug prediction.鉴定和分析激素性股骨头坏死相关的线粒体中央基因，并进行药物预测。
Front Endocrinol (Lausanne). 2024 Feb 7;15:1341366. doi: 10.3389/fendo.2024.1341366. eCollection 2024.
5
Effects of external environment on promoter methylation of PIK3R5 and related pathway regulation in steroid-induced femoral head necrosis.环境因素对激素诱导性股骨头坏死中 PIK3R5 启动子甲基化及其相关通路调控的影响。
Environ Res. 2023 Dec 1;238(Pt 1):117116. doi: 10.1016/j.envres.2023.117116. Epub 2023 Sep 12.
6
Downregulating STAT1/caspase-3 signaling with fludarabine to alleviate progression in a rat model of steroid-induced avascular necrosis of the femoral head.用氟达拉滨下调 STAT1/caspase-3 信号通路以减轻激素诱导性股骨头坏死大鼠模型中的进展。
J Biochem Mol Toxicol. 2019 Apr;33(4):e22265. doi: 10.1002/jbt.22265. Epub 2018 Dec 1.
7
Identification of potential autophagy-related genes in steroid-induced osteonecrosis of the femoral head via bioinformatics analysis and experimental verification.通过生物信息学分析和实验验证鉴定激素性股骨头坏死中潜在的自噬相关基因。
J Orthop Surg Res. 2022 Feb 12;17(1):86. doi: 10.1186/s13018-022-02977-x.
8
Bioinformatics proved the existence of potential hub genes activating autophagy to participate in cartilage degeneration in osteonecrosis of the femoral head.生物信息学证实了潜在的枢纽基因的存在，这些基因可以激活自噬，从而参与股骨头坏死中的软骨退化。
J Mol Histol. 2024 Aug;55(4):539-554. doi: 10.1007/s10735-024-10200-w. Epub 2024 May 17.
9
Comprehensive analysis of pivotal biomarkers, immune cell infiltration and therapeutic drugs for steroid-induced osteonecrosis of the femoral head.全面分析关键生物标志物、免疫细胞浸润和治疗药物在激素性股骨头坏死中的作用。
Bioengineered. 2021 Dec;12(1):5971-5984. doi: 10.1080/21655979.2021.1972081.
10
Upregulation of microRNA-320 decreases the risk of developing steroid-induced avascular necrosis of femoral head by inhibiting CYP1A2 both in vivo and in vitro.miRNA-320 的上调通过抑制 CYP1A2 的表达，在体内和体外均降低了类固醇诱导的股骨头缺血性坏死的风险。
Gene. 2018 Jun 20;660:136-144. doi: 10.1016/j.gene.2018.03.045. Epub 2018 Mar 15.

引用本文的文献

1
Mesenchymal stem cells: A new strategy for the treatment of femoral head necrosis.间充质干细胞：治疗股骨头坏死的新策略。
Regen Ther. 2025 Jul 23;30:421-429. doi: 10.1016/j.reth.2025.07.008. eCollection 2025 Dec.

本文引用的文献

1
Macrophage Polarization and the Regulation of Bone Immunity in Bone Homeostasis.巨噬细胞极化与骨稳态中骨免疫的调节
J Inflamm Res. 2023 Aug 22;16:3563-3580. doi: 10.2147/JIR.S423819. eCollection 2023.
2
BRD9-mediated chromatin remodeling suppresses osteoclastogenesis through negative feedback mechanism.BRD9 通过负反馈机制介导染色质重塑抑制破骨细胞生成。
Nat Commun. 2023 Mar 14;14(1):1413. doi: 10.1038/s41467-023-37116-5.
3
Bioactive compounds modulating Toll-like 4 receptor (TLR4)-mediated inflammation: pathways involved and future perspectives.
调节 Toll 样受体 4（TLR4）介导的炎症的生物活性化合物：涉及的途径和未来展望。
Nutr Res. 2022 Nov;107:96-116. doi: 10.1016/j.nutres.2022.09.001. Epub 2022 Sep 9.
4
Activation and regulation mechanisms of NOD-like receptors based on structural biology.基于结构生物学的 NOD 样受体的激活和调控机制。
Front Immunol. 2022 Sep 15;13:953530. doi: 10.3389/fimmu.2022.953530. eCollection 2022.
5
The Role of Inflammasome NLPR3 in the Development and Therapy of Periodontitis.NLRP3 炎性小体在牙周炎发病机制和治疗中的作用。
Int J Med Sci. 2022 Sep 21;19(10):1603-1614. doi: 10.7150/ijms.74575. eCollection 2022.
6
The Risk of Avascular Necrosis Following the Stabilization of Femoral Neck Fractures: A Systematic Review and Meta-Analysis.股骨颈骨折固定后发生缺血性坏死的风险：系统评价和荟萃分析。
Int J Environ Res Public Health. 2022 Aug 15;19(16):10050. doi: 10.3390/ijerph191610050.
7
Activation and Function of NLRP3 Inflammasome in Bone and Joint-Related Diseases.NLRP3 炎性小体在骨与关节相关疾病中的激活与作用。
Int J Mol Sci. 2022 May 11;23(10):5365. doi: 10.3390/ijms23105365.
8
Treatment of non-traumatic avascular necrosis of the femoral head (Review).非创伤性股骨头缺血性坏死的治疗（综述）
Exp Ther Med. 2022 May;23(5):321. doi: 10.3892/etm.2022.11250. Epub 2022 Mar 10.
9
Toll-like receptor 4 (TLR4) inhibitors: Current research and prospective.Toll样受体4（TLR4）抑制剂：当前研究与展望
Eur J Med Chem. 2022 May 5;235:114291. doi: 10.1016/j.ejmech.2022.114291. Epub 2022 Mar 15.
10
Decreased serum CXCL12/SDF-1 concentrations may reflect disease severity of non-traumatic osteonecrosis of femoral head.血清CXCL12/SDF-1浓度降低可能反映非创伤性股骨头坏死的疾病严重程度。
Clin Chim Acta. 2022 Apr 1;529:87-95. doi: 10.1016/j.cca.2022.02.009. Epub 2022 Feb 17.