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突触-线粒体运输:神经适应与退变机制

Synaptic-mitochondrial transport: mechanisms in neural adaptation and degeneration.

作者信息

Ding Yang, Yang Huan, Gao Jie, Tang Can, Peng Yu-Yuan, Ma Xin-Mei, Li Sen, Wang Hai-Yan, Lu Xiu-Min, Wang Yong-Tang

机构信息

College of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing, 400054, China.

State Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing, 400042, China.

出版信息

Mol Cell Biochem. 2025 Jun;480(6):3399-3411. doi: 10.1007/s11010-025-05209-y. Epub 2025 Jan 22.

DOI:10.1007/s11010-025-05209-y
PMID:39841406
Abstract

Synaptic plasticity is the basis for the proper functioning of the central nervous system. Synapses are the contact points between neurons and are crucial for information transmission, the structure and function of synapses change adaptively based on the different activities of neurons, thus affecting processes such as learning, memory, and neural development and repair. Synaptic activity requires a large amount of energy provided by mitochondria. Mitochondrial transport proteins regulate the positioning and movement of mitochondria to maintain normal energy metabolism. Recent studies have shown a close relationship between mitochondrial transport proteins and synaptic plasticity, providing a new direction for the study of adaptive changes in the central nervous system and new targets for the treatment of neurodegenerative diseases.

摘要

突触可塑性是中枢神经系统正常运作的基础。突触是神经元之间的接触点,对信息传递至关重要,突触的结构和功能会根据神经元的不同活动而适应性地改变,从而影响学习、记忆以及神经发育和修复等过程。突触活动需要线粒体提供大量能量。线粒体转运蛋白调节线粒体的定位和移动,以维持正常的能量代谢。最近的研究表明线粒体转运蛋白与突触可塑性之间存在密切关系,为中枢神经系统适应性变化的研究提供了新方向,也为神经退行性疾病的治疗提供了新靶点。

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Synaptic-mitochondrial transport: mechanisms in neural adaptation and degeneration.突触-线粒体运输:神经适应与退变机制
Mol Cell Biochem. 2025 Jun;480(6):3399-3411. doi: 10.1007/s11010-025-05209-y. Epub 2025 Jan 22.
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Mitochondrial potassium channels and uncoupling proteins in synaptic plasticity and neuronal cell death.线粒体钾通道与解偶联蛋白在突触可塑性和神经元细胞死亡中的作用
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本文引用的文献

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PSAT1 promotes the progression of colorectal cancer by regulating Hippo-YAP/TAZ-ID1 axis via AMOT.PSAT1通过AMOT调控Hippo-YAP/TAZ-ID1轴促进结直肠癌进展。
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HMGB1 Promotes Accelerated Fracture Healing in Traumatic Brain Injury through PINK1/Parkin-Mediated Mitochondrial Autophagy.高迁移率族蛋白B1通过PINK1/帕金介导的线粒体自噬促进创伤性脑损伤中骨折的加速愈合。
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Intestinal flora plays a role in the progression of hepatitis-cirrhosis-liver cancer.肠道菌群在肝炎-肝硬化-肝癌的进展中发挥作用。
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Synaptic degeneration in Alzheimer disease.阿尔茨海默病中的突触退化
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CRISPR/Cas9 Mediated Therapeutic Approach in Huntington's Disease.CRISPR/Cas9 介导的亨廷顿病治疗方法。
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Energy matters: presynaptic metabolism and the maintenance of synaptic transmission.能量很重要:突触前代谢与突触传递的维持。
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Insights into the Pathogenesis of Neurodegenerative Diseases: Focus on Mitochondrial Dysfunction and Oxidative Stress.神经退行性疾病发病机制的研究进展:聚焦线粒体功能障碍与氧化应激。
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