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自噬对肝衰竭的保护作用机制与临床价值

胡洋洋 张兴 罗越 王亚东 赵彩彦

引用本文:
Citation:

自噬对肝衰竭的保护作用机制与临床价值

DOI: 10.3969/j.issn.1001-5256.2023.10.030
基金项目: 

河北省自然科学基金 (H2020206036);

河北省科技厅重点研发计划项目 (21377756D)

利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:胡洋洋负责查阅文献,撰写文章;张兴、罗越负责校对文章;王亚东负责指导立题及修改;赵彩彦负责审阅文章等。
详细信息
    通信作者:

    王亚东, wangyadong8060@126.com (ORCID: 0000-0003-0140-0674)

Advances in the protective mechanism and clinical implications of autophagy in liver failure

Research funding: 

Natural Science Foundation of Hebei Province (H2020206036);

Key Research and Development Project of Hebei Province (21377756D)

More Information
  • 摘要: 肝衰竭是一类严重临床肝病症候群,病情危重、病死率高,除肝移植外,缺乏理想的根治性治疗手段。肝衰竭发病机制复杂且尚未完全阐明,多种影响肝细胞坏死与再生平衡的因素参与其中。本文总结了自噬这一维持细胞稳态的关键性途径,指出自噬通过调控NLRP3炎症小体活化、对抗氧化应激、抑制细胞凋亡等多种方式在肝衰竭发病机制中发挥重要保护作用。同时认为外泌体、过氧化物酶体增殖物激活受体α等以自噬为靶点的分子信号通路参与拮抗肝衰竭发生、发展,将成为肝衰竭分子靶向治疗的重要思路和方向。

     

  • 图  1  自噬在肝衰竭中的保护作用机制

    注: ARE,抗氧化反应元件;ASC,凋亡相关斑点样蛋白;GCLC,谷氨酸-半胱氨酸连接酶催化亚基;GSTM,谷胱甘肽-S-转移酶Mu;HO-1,血红素加氧酶-1;Keap1, Kelch样ECH相关蛋白1;Nrf2,核因子E2相关因子2;PINK1,PTEN诱导性激酶蛋白1;TXNIP,硫氧还蛋白相互作用蛋白;ΔΨm,线粒体膜电位。

    Figure  1.  The protective mechanism of autophagy in liver failure

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  • 收稿日期:  2023-02-08
  • 出版日期:  2023-10-30
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