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坏死性凋亡在肝纤维化中的作用

吴旋 李晖 董海舰 杨希坤 王凯鑫

引用本文:
Citation:

坏死性凋亡在肝纤维化中的作用

DOI: 10.12449/JCH240827
基金项目: 

国家自然科学基金面上项目 (82274323)

利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:吴旋负责撰写论文;董海舰、杨希坤、王凯鑫参与查找文献,修改论文;李晖负责拟定写作思路,指导论文撰写并最后定稿。
详细信息
    通信作者:

    李晖, 1400124746@qq.com (ORCID: 0000-0002-5919-1396)

The role of necroptosis in liver fibrosis

Research funding: 

General Project of National Natural Science Foundation of China (82274323)

More Information
    Corresponding author: LI Hui, 1400124746@qq.com (ORCID: 0000-0002-5919-1396)
  • 摘要: 肝纤维化作为各种慢性肝病向肝硬化发展的关键环节,影响其预后与转归。坏死性凋亡是一种新型的程序性细胞死亡模式,已被证明在多种疾病的病理生理中发挥重要作用,同样也被认为是改善肝纤维化的潜在靶点。不同类型的肝内细胞(包括肝细胞、肝星状细胞、肝巨噬细胞及肝窦内皮细胞)发生坏死性凋亡,可对肝纤维化发挥促进或抑制作用,本文着重阐述上述作用机制,并讨论靶向坏死性凋亡介导的肝纤维化的治疗策略。

     

  • 表  1  肝内细胞坏死性凋亡与肝纤维化的关系

    Table  1.   Relationship between intrahepatic cell necroptosis and liver fibrosis

    肝内细胞类型

    发生坏死性凋亡后

    对肝纤维化的影响

    主要作用机制 治疗思路
    肝细胞 促进 促进促炎因子DAMP释放,诱导HSC活化 抑制其坏死性凋亡
    HSC 抑制 直接抑制HSC活化 靶向促进其发生坏死性凋亡
    M1巨噬细胞 抑制 促进促炎因子DAMP释放,诱导HSC活化 靶向促进其发生坏死性凋亡
    M2巨噬细胞 促进 吞噬死亡肝细胞,清除促炎因子,抑制HSC活化 抑制其坏死性凋亡
    肝窦内皮细胞 促进 调节肝脏内环境能力受损,促进HSC活化 抑制其坏死性凋亡
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