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铁死亡的发生机制及在肝脏疾病中的作用

张飞宇 阿迪拉·亚克普 赵金明 高沿航

引用本文:
Citation:

铁死亡的发生机制及在肝脏疾病中的作用

DOI: 10.3969/j.issn.1001-5256.2021.06.049
基金项目: 

国家自然科学基金 (81972265);

国家重点研发计划“精准医学研究”专项 (2017YFC0908103);

“艾滋病和病毒性肝炎等重大传染病防治”国家科技重大专项 (2017ZX10202202);

“艾滋病和病毒性肝炎等重大传染病防治”国家科技重大专项 (2018ZX10302206);

吉林省自然科学基金 (20200201324JC)

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:张飞宇负责选题,收集分析资料,撰写文章;阿迪拉·亚克普、赵金明参与选题,收集资料;高沿航教授拟定写作思路,指导撰写文章,提供修改意见并最终定稿。
详细信息
    作者简介:

    张飞宇(1995—),男,主要从事肝胆胰腺疾病研究

    通信作者:

    高沿航,yanhang@mail.jlu.edu.cn

  • 中图分类号: R575

Mechanism of ferroptosis and its role in liver diseases

  • 摘要: 铁死亡是新近发现的一种铁依赖性、脂质过氧化物集聚导致的调节性细胞死亡,其形态学特征为线粒体体积缩小、膜密度增加和线粒体减少或消失。发生机制主要与铁代谢紊乱、氨基酸抗氧化系统失衡、脂质过氧化物集聚有关。研究显示,铁死亡在不同的肝脏疾病背景下扮演不同角色,铁死亡的发生可参与多种肝脏炎症疾病进展,也可抑制肝纤维化形成、肝癌发生及索拉非尼耐药。总结了铁死亡发生机制及其在肝脏疾病中的作用和进展,旨在为肝脏疾病的进一步研究与治疗提供参考。

     

  • 图  1  4种细胞死亡方式机制图

    注:a, 肝细胞的外源性凋亡机制; b, 坏死性凋亡机制; c, 焦亡机制; d, 自噬机制。

    图  2  铁死亡发生机制图

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出版历程
  • 收稿日期:  2020-11-30
  • 录用日期:  2020-12-29
  • 出版日期:  2021-06-20
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