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细胞因子信号转导抑制因子1在肝脏炎症性疾病发生发展中的作用机制

吴霞 朱晓宁 张玉蓉 尹玥 彭孟云 郑丁 汪静

引用本文:
Citation:

细胞因子信号转导抑制因子1在肝脏炎症性疾病发生发展中的作用机制

DOI: 10.3969/j.issn.1001-5256.2021.04.055
基金项目: 

国家自然科学基金 (81704053);

泸州市科学技术和知识产权局科技计划 (泸市科知〔2017〕241号)

利益冲突声明:所有作者均声明不存在利益冲突。
作者贡献声明:吴霞负责资料分析,撰写论文;朱晓宁、张玉蓉、尹玥、彭孟云、郑丁参与收集数据,修改论文;汪静负责拟定写作思路,指导撰写文章并最后定稿。
详细信息
    作者简介:

    吴霞(1995—),女,主要从事中西医结合肝病防治研究

    通信作者:

    汪静,lywj68@126.com

  • 中图分类号: R575

Mechanism of action of suppressor of cytokine signaling 1 in the development and progression of liver inflammatory diseases

  • 摘要: 肝脏炎症性疾病的发生与自身免疫和炎症反应有关,细胞因子信号转导抑制因子1(SOCS1)作为一种细胞信号的负反馈调节因子,其在炎症性疾病的发生发展中起到关键作用。介绍了SOCS1在自身免疫与炎症反应中的作用机制,简述其在肝脏炎症性疾病如病毒性肝炎、非酒精性脂肪性肝炎等疾病发生、发展中的作用。分析表明SOCS1在炎症反应中的异常表达与细胞因子受体、Toll样受体和激素受体信号的调控有关,从而导致炎症性疾病的发生,因此SOCS1作为肝脏炎症性疾病诊断和治疗的辅助手段具有潜在的发展前景。

     

  • 图  1  SOCS1的结构及功能

    注:a,SOCS1蛋白结构;b,SOCS1蛋白募集E3泛素酶体机制。

    图  2  SOCS1在乙型肝炎、丙型肝炎中的作用机制

    表  1  SOCS1在不同病因肝脏炎症中可能的作用机制

    病因分类 病因相关SOCS1调节因子 SOCS1表达 调控信号通路 机制/结局 参考文献
    HBV HBcAg18-27蛋白 降低 IFNγ/STAT1 Th1/Th2增加,HBV降低 Tang等[26]
    HBsAg 增加 TLR IFNα表达增加 Xu等[27]
    HCV HCV蛋白、IFN 增加 JAK/STAT 清除HCV Singh等[22]
    肝脏缺血再灌注 miRNA-155 降低 NF-κB TNFα、IL-6表达增加 Tan等[35]
    PBC VDR 降低 miRNA-155-SOCS1 miRNA-155表达上调、持续炎症 Yuan等[36]
    NAFLD 早期生长反应蛋2 增加 JAK2/STAT3/SOCS1 脂肪变性 Kempinska-Podhorodecka等[37]
    熊去氧胆酸 降低 NF-κB/STAT3 FFA、TG分泌降低 Chen等[38]
    利莫那班 降低 AMPK磷酸化 改善脂肪变性 Chang等[39]
    药物性肝损伤 雷公藤内酯醇 增加 Notch信号通路 ALT、AST分泌增加 Wang等[40]
    血吸虫肝病 科利拉金 增加 IL-13/STAT6 肉芽肿减小 Du等[41]
    肝衰竭 脂多糖/D-半乳糖胺 增加 JAK2/STAT1 抑制TLR4通路 Li等[42]
    注:AMPK,AMP依赖的蛋白激酶;FFA,游离脂肪酸;TG,总胆固醇。
    下载: 导出CSV
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  • 收稿日期:  2020-09-19
  • 录用日期:  2020-10-10
  • 出版日期:  2021-04-20
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