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中华诊断学电子杂志 ›› 2022, Vol. 10 ›› Issue (03) : 211 -215. doi: 10.3877/cma.j.issn.2095-655X.2022.03.013

综述

铁死亡在阿尔茨海默病发病机制中的研究进展
刘倩1, 李鑫1, 刘欣1, 苑金香2,†()   
  1. 1. 272067　济宁医学院基础医学院
    2. 272067　济宁医学院协同创新中心
  • 收稿日期:2022-06-29 出版日期:2022-08-26
  • 通信作者: 苑金香

Research progress of ferroptosis in the pathogenesis of Alzheimer′s disease

Qian Liu1, Xin Li1, Xin Liu1, Jinxiang Yuan2,†()   

  1. 1. College of Basic Medicine, Jining Medical University, Jining 272067, China
    2. Collaborative Innovation Center, Jining Medical University, Jining 272067, China
  • Received:2022-06-29 Published:2022-08-26
  • Corresponding author: Jinxiang Yuan
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刘倩, 李鑫, 刘欣, 苑金香. 铁死亡在阿尔茨海默病发病机制中的研究进展[J/OL]. 中华诊断学电子杂志, 2022, 10(03): 211-215.

Qian Liu, Xin Li, Xin Liu, Jinxiang Yuan. Research progress of ferroptosis in the pathogenesis of Alzheimer′s disease[J/OL]. Chinese Journal of Diagnostics(Electronic Edition), 2022, 10(03): 211-215.

阿尔茨海默病(AD)是常见的神经退行性疾病，其发病与年龄增长密切相关。随着人口老龄化的加剧，AD的发病率逐年上升。铁死亡作为一种不同于细胞凋亡、坏死和自噬的新型细胞死亡形式，其的主要特征包括铁依赖性的脂质过氧化、谷胱甘肽耗竭和铁超载。谷胱甘肽过氧化物酶4(GPX4)是一种硒蛋白，具有抗脂质过氧化的作用，是铁死亡中的关键调节因子。脂质过氧化、铁代谢紊乱以及硒缺乏介导的铁死亡均展现出强烈的AD相关性。笔者主要总结铁死亡在AD中的关键机制及研究进展，并展望铁死亡在AD治疗方面的作用。

关键词: 铁死亡, 阿尔茨海默病, 谷胱甘肽过氧化物酶4

Alzheimer′s disease (AD) is a common neurodegenerative disease which is closely related to aging. AD is becoming more common with the aggravation of population aging, the incidence rate of it increases year by year. Ferroptosis is a type of cell death distinct from apoptosis, necrosis, and autophagy. Ferroptosis is distinguished by iron-dependent lipid peroxidation, glutathione depletion, and iron overload. Glutathione peroxidase 4 (GPX4) is a selenoprotein with anti-lipid peroxidation and is a key regulator in ferroptosis. Lipid peroxidation, iron metabolism disruption, and ferroptosis caused by selenium deficiency demonstrate close relationship with AD. This paper summarizes the key mechanisms and research progress of ferroptosis in AD, as well as the prospects of ferroptosis in the treatment of AD.

Key words: Ferroptosis, Alzheimer disease, Glutathione peroxidase 4
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