中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2019, Vol. 14 ›› Issue (5): 749-756.doi: 10.4103/1673-5374.249218

• 综述:退行性病与再生 • 上一篇    下一篇

线粒体自噬与氧化应激和神经退行性病变有关

  

  • 出版日期:2019-05-15 发布日期:2019-05-15
  • 基金资助:

     韩国科学，ICT和未来计划部国家基础科学研究计划

Mitophagy links oxidative stress conditions and neurodegenerative diseases

Ulfuara Shefa 1 , Na Young Jeong 2 , In Ok Song 3 , Hyung-Joo Chung 4 , Dokyoung Kim 1, 5 , Junyang Jung 1, 5 , Youngbuhm Huh 1, 5   

  1. 1 Department of Biomedical Science, Graduate School, Kyung Hee University, Seoul, South Korea
    2 Department of Anatomy and Cell Biology, College of Medicine, Dong-A University, Busan, South Korea
    3 Department of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Cheil General Hospital, Dankook University College of Medicine, Seoul, South Korea
    4 Department of Anesthesiology and Pain Medicine, College of Medicine, Kosin University, Busan, South Korea
    5 Department of Anatomy and Neurobiology, College of Medicine, Kyung Hee University, Seoul, South Korea
  • Online:2019-05-15 Published:2019-05-15
  • Contact: Junyang Jung, MD, PhD, jjung@khu.ac.kr; Youngbuhm Huh, MD, PhD, ybhuh@khu.ac.kr.
  • Supported by:

    This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT and Future Planning, No. 2018R1C1B5029745 (to HJC), 2011-0030072 (to YH), 2018R1D1A1B07040282 (to JJ), and 2018R1A2B6001123 (to NYJ).

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摘要：

影响线粒体自噬激活的刺激因素包括缺氧、能量应激和氧化磷酸化活性的增加。适当调节线粒体自噬对维持体内平衡至关重要;相反，通过线粒体自噬导致的线粒体去除不充分可导致氧化物质的产生，包括活性氧和活性氮，从而引起各种神经退行性疾病，例如阿尔茨海默病、帕金森病、亨廷顿病和肌萎缩侧索硬化症。由于线粒体自噬对正常身体功能的维持至关重要，因而通过靶向线粒体途径，可以改善这些疾病状况。这篇综述讨论了线粒体自噬在体内平衡中的重要作用以及它的失调如何导致神经变性；同时还讨论了如何通过靶向线粒体自噬途径对抗氧化应激，从而有助于治疗神经退行性疾病。

orcid: 0000-0003-3946-5406(Junyang Jung)
           0000-0002-7687-0374(Youngbuhm Huh)

关键词: 线粒体自噬, 阿尔茨海默病, 帕金森病, 亨廷顿氏病, 肌萎缩侧索硬化症, 氧化应激, 活性氧, 活性氮, 神经退行性疾病, 神经再生

Abstract:

Mitophagy is activated by a number of stimuli, including hypoxia, energy stress, and increased oxidative phosphorylation activity. Mitophagy is associated with oxidative stress conditions and central neurodegenerative diseases. Proper regulation of mitophagy is crucial for maintaining homeostasis; conversely, inadequate removal of mitochondria through mitophagy leads to the generation of oxidative species, including reactive oxygen species and reactive nitrogen species, resulting in various neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. These diseases are most prevalent in older adults whose bodies fail to maintain proper mitophagic functions to combat oxidative species. As mitophagy is essential for normal body function, by targeting mitophagic pathways we can improve these disease conditions. The search for effective remedies to treat these disease conditions is an ongoing process, which is why more studies are needed. Additionally, more relevant studies could help establish therapeutic conditions, which are currently in high demand. In this review, we discuss how mitophagy plays a significant role in homeostasis and how its dysregulation causes neurodegeneration. We also discuss how combating oxidative species and targeting mitophagy can help treat these neurodegenerative diseases.

Key words: nerve regeneration, mitophagy, central nervous system, Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, oxidative species, reactive oxygen species, reactive nitrogen species