程序性坏死发生机制在帕金森病中作用的研究进展

doi:10.19586/j.2095-2341.2022.0204

生物技术进展 ›› 2023, Vol. 13 ›› Issue (3): 406-411.DOI: 10.19586/j.2095-2341.2022.0204

程序性坏死发生机制在帕金森病中作用的研究进展

邱思元(), 闫立地(), 赵文婧, 赵金玉, 段育阳, 王桐

大庆师范学院生物工程学院，黑龙江大庆 163712

收稿日期:2022-12-02 接受日期:2023-03-03 出版日期:2023-05-25 发布日期:2023-06-12
通讯作者: 闫立地
作者简介:邱思元 E-mail： 1178735617@qq.com；
基金资助:
黑龙江省自然科学基金联合引导项目(LH2019C071)

Research Progress on the Role of Necroptosis Development Mechanism in Parkinson's Disease

Siyuan QIU(), Lidi YAN(), Wenjing ZHAO, Jinyu ZHAO, Yuyang DUAN, Tong WANG

College of Bioengineering，Daqing Normal University，Heilongjiang Daqing 163712，China

Received:2022-12-02 Accepted:2023-03-03 Online:2023-05-25 Published:2023-06-12
Contact: Lidi YAN

摘要/Abstract

摘要：

细胞程序性坏死是一种新发现的细胞死亡方式，该死亡方式兼具细胞凋亡与细胞坏死特征。近年来研究显示，程序性坏死在帕金森疾病发展过程中发挥重要作用。通过总结细胞程序性坏死的重要因子，如诱导因子（TNF-α和Caspase-8）、轴心蛋白（RIPK1、RIPK3、MLKL）和其他因素（炎症与氧化应激），讨论了程序性坏死发生机制和帕金森病之间的关系，以期为研究帕金森病发病机制与研发相关药物提供参考。

关键词: 细胞程序性坏死, 帕金森病, RIPK1-RIPK3-MLKL复合体

Abstract:

Necroptosis is a newfound form of cell death that combines apoptosis and cell necrosis. Recent studies have shown that necroptosis plays an important role in the development of Parkinson's disease. By summarizing important factors of necroptosis， such as inducible factors （TNF-α and Caspase-8）， axial proteins （RIPK1， RIPK3， MLKL）， and other factors （inflammation and oxidative stress）， this paper discussed the relationship between the pathogenesis of necroptosis and Parkinson's disease， in order to provide reference for the pathogenesis of Parkinson's disease and related drug development.

Key words: necroptosis, Parkinson's disease, RIPK1-RIPK3-MLKL complex

中图分类号:

R742.5

邱思元, 闫立地, 赵文婧, 赵金玉, 段育阳, 王桐. 程序性坏死发生机制在帕金森病中作用的研究进展[J]. 生物技术进展, 2023, 13(3): 406-411.

Siyuan QIU, Lidi YAN, Wenjing ZHAO, Jinyu ZHAO, Yuyang DUAN, Tong WANG. Research Progress on the Role of Necroptosis Development Mechanism in Parkinson's Disease[J]. Current Biotechnology, 2023, 13(3): 406-411.

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程序性坏死发生机制在帕金森病中作用的研究进展

Research Progress on the Role of Necroptosis Development Mechanism in Parkinson's Disease

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