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细胞器相互作用在肝纤维化进展中的作用机制及中药防治策略

郑瑗瑗 赵晨露 张丽慧 刘素彤 赵文霞

引用本文:
Citation:

细胞器相互作用在肝纤维化进展中的作用机制及中药防治策略

DOI: 10.12449/JCH260329
基金项目: 

国家自然科学基金青年基金项目 (82505480);

河南中医药大学博士科研启动基金 (2023BSJJ035)

利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:郑瑗瑗负责资料分析,撰写论文;赵晨露负责拟定写作思路;张丽慧、刘素彤负责修改论文;赵文霞负责指导撰写文章并最后定稿。
详细信息
    通信作者:

    赵文霞, zhao-wenxia@163.com (ORCID: 0000-0002-0592-3504)

Mechanism of action of organelle interactions in the progression of liver fibrosis and traditional Chinese medicine prevention and treatment strategies

Research funding: 

Natural Science Foundation of China Young Scientists Fund (82505480);

Doctoral Research Startup Fund of Henan University of Chinese Medicine (2023BSJJ035)

More Information
  • 摘要: 肝纤维化是多种慢性肝病进展至肝硬化的核心病理阶段,其发生发展主要依赖于肝星状细胞的活化及胶原纤维的异常沉积。近年研究发现,肝星状细胞的活化受到多种细胞器(包括线粒体、内质网、高尔基体、溶酶体和过氧化物酶体等)彼此间复杂相互作用的调控,这些互相作用共同影响能量代谢、蛋白质合成与折叠、活性氧平衡及自噬等关键细胞过程,进而参与肝纤维化进展。同时,具有多靶点协同作用的中药及其活性成分受到研究者的广泛关注。本文从细胞器间相互作用的角度出发,系统阐述其在肝纤维化进展中的具体作用机制,并重点综述中药如何通过调控上述细胞器功能及其互作网络,抑制肝星状细胞活化及胶原生成,从而发挥抗肝纤维化效应,以期为深入解析肝纤维化病理机制及开发中药新型干预策略提供理论依据。

     

  • 注: HSC,肝星状细胞;COPⅠ,包被蛋白Ⅰ;COPⅡ,包被蛋白Ⅱ;TCA循环,三羧酸循环;PS,磷脂酰丝氨酸;Mfn2,线粒体融合蛋白2;ER stress,内质网应激;PERK,蛋白激酶R样内质网激酶;ATF6α,激活转录因子6α;IRE1α,肌醇需求蛋白1α;UPR,未折叠蛋白质反应;ERLAD,ER-溶酶体相关降解途径;Syt7,溶酶体突触结合蛋白Ⅶ;MCS,膜接触位点;PI(4,5)P,磷脂酰肌醇-4,5-二磷酸;CTSB,组织蛋白酶B;LMP,溶酶体膜透化;PAI-1,纤溶酶原激活物抑制剂-1;Col1α1,Ⅰ型胶原α1。

    图  1  细胞器间相互作用影响肝纤维化进展

    Figure  1.  Intercellular organelle interactions in liver fibrosis progression

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