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轴突退变与再生中的线粒体行为

Mitochondrial Behavior in Axon Degeneration and Regeneration.

作者信息

Wang Biyao, Huang Minghao, Shang Dehao, Yan Xu, Zhao Baohong, Zhang Xinwen

机构信息

The VIP Department, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Diseases, Shenyang, China.

Center of Implant Dentistry, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Diseases, Shenyang, China.

出版信息

Front Aging Neurosci. 2021 Mar 8;13:650038. doi: 10.3389/fnagi.2021.650038. eCollection 2021.

DOI:10.3389/fnagi.2021.650038
PMID:33762926
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7982458/
Abstract

Mitochondria are organelles responsible for bioenergetic metabolism, calcium homeostasis, and signal transmission essential for neurons due to their high energy consumption. Accumulating evidence has demonstrated that mitochondria play a key role in axon degeneration and regeneration under physiological and pathological conditions. Mitochondrial dysfunction occurs at an early stage of axon degeneration and involves oxidative stress, energy deficiency, imbalance of mitochondrial dynamics, defects in mitochondrial transport, and mitophagy dysregulation. The restoration of these defective mitochondria by enhancing mitochondrial transport, clearance of reactive oxidative species (ROS), and improving bioenergetic can greatly contribute to axon regeneration. In this paper, we focus on the biological behavior of axonal mitochondria in aging, injury (e.g., traumatic brain and spinal cord injury), and neurodegenerative diseases (Alzheimer's disease, AD; Parkinson's disease, PD; Amyotrophic lateral sclerosis, ALS) and consider the role of mitochondria in axon regeneration. We also compare the behavior of mitochondria in different diseases and outline novel therapeutic strategies for addressing abnormal mitochondrial biological behavior to promote axonal regeneration in neurological diseases and injuries.

摘要

线粒体是负责生物能量代谢、钙稳态和信号传递的细胞器,由于神经元能量消耗高,这些功能对神经元至关重要。越来越多的证据表明,线粒体在生理和病理条件下的轴突退变和再生中起关键作用。线粒体功能障碍发生在轴突退变的早期,涉及氧化应激、能量缺乏、线粒体动力学失衡、线粒体运输缺陷和线粒体自噬失调。通过增强线粒体运输、清除活性氧(ROS)和改善生物能量来恢复这些有缺陷的线粒体,可极大地促进轴突再生。在本文中,我们关注轴突线粒体在衰老、损伤(如创伤性脑损伤和脊髓损伤)以及神经退行性疾病(阿尔茨海默病、AD;帕金森病、PD;肌萎缩侧索硬化症、ALS)中的生物学行为,并探讨线粒体在轴突再生中的作用。我们还比较了线粒体在不同疾病中的行为,并概述了针对异常线粒体生物学行为的新型治疗策略,以促进神经疾病和损伤中的轴突再生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b3/7982458/42fdafbf5c9a/fnagi-13-650038-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b3/7982458/42fdafbf5c9a/fnagi-13-650038-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b3/7982458/42fdafbf5c9a/fnagi-13-650038-g0001.jpg

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Oligodendroglial glycolytic stress triggers inflammasome activation and neuropathology in Alzheimer's disease.少突胶质细胞糖酵解应激引发阿尔茨海默病中的炎症小体激活和神经病理学。
Sci Adv. 2020 Dec 4;6(49). doi: 10.1126/sciadv.abb8680. Print 2020 Dec.
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Metabolic Dysregulation Contributes to the Progression of Alzheimer's Disease.
线粒体自噬:脊髓损伤病理生理学及治疗中的关键调节因子
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Mitochondrial dynamics reveal potential to facilitate axonal regeneration after spinal cord injury.线粒体动力学显示出促进脊髓损伤后轴突再生的潜力。
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Mitochondria-Nuclear Crosstalk: Orchestrating mtDNA Maintenance.线粒体-细胞核相互作用:协调线粒体DNA的维持
Environ Mol Mutagen. 2025 Jun;66(5):222-242. doi: 10.1002/em.70013. Epub 2025 May 26.
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The neuroimmune nexus: unraveling the role of the mtDNA-cGAS-STING signal pathway in Alzheimer's disease.神经免疫联系:揭示线粒体DNA-环鸟苷酸-腺苷酸合成酶-干扰素基因刺激蛋白信号通路在阿尔茨海默病中的作用
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