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突触融合蛋白失活可增强轴突线粒体运输,改善脊髓损伤。

Syntaphilin Inactivation Can Enhance Axonal Mitochondrial Transport to Improve Spinal Cord Injury.

机构信息

Department of Histology and Embryology, Medical College, Shaoxing University, Shaoxing, 312000, Zhejiang, China.

Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou, China.

出版信息

Mol Neurobiol. 2023 Nov;60(11):6556-6565. doi: 10.1007/s12035-023-03494-6. Epub 2023 Jul 17.

DOI:10.1007/s12035-023-03494-6
PMID:37458986
Abstract

Mitochondria are important organelle of eukaryotic cells. They consists of a large number of different proteins that provide most of the ATP and supply power for the growth, function, and regeneration of neurons. Therefore, smitochondrial transport ensures that adequate ATP is supplied for metabolic activities. Spinal cord injury (SCI), a detrimental condition, has high morbidity and mortality rates. Currently, the available treatments only provide symptomatic relief for long-term disabilities. Studies have implicated mitochondrial transport as a critical factor in axonal regeneration. Hence, enhancing mitochondrial transports could be beneficial for ameliorating SCI. Syntaphilin (Snph) is a mitochondrial docking protein that acts as a "static anchor," and its inhibition enhances mitochondrial transports. Therefore, Snph as a key mediator of mitochondrial transports, may contribute to improving axonal regeneration following SCI. Herein, we examine Snph's biological effects and its relation to mitochondrial pathway. Then, we elaborate on mitochondrial transports after SCI, the possible role of Snph in SCI, and some possible therapeutic approaches by Snph.

摘要

线粒体是真核细胞的重要细胞器。它们由大量不同的蛋白质组成,为神经元的生长、功能和再生提供大部分的 ATP 并提供动力。因此,线粒体的运输确保了足够的 ATP 供应来进行代谢活动。脊髓损伤 (SCI) 是一种有害的疾病,其发病率和死亡率都很高。目前,现有的治疗方法仅能为长期残疾提供对症缓解。研究表明,线粒体运输是轴突再生的关键因素。因此,增强线粒体的运输可能有助于改善 SCI。Syntaphilin (Snph) 是一种线粒体对接蛋白,它作为一种“静态锚”,其抑制作用增强了线粒体的运输。因此,Snph 作为线粒体运输的关键介质,可能有助于改善 SCI 后的轴突再生。本文中,我们研究了 Snph 的生物学作用及其与线粒体途径的关系。然后,我们详细阐述了 SCI 后线粒体的运输、Snph 在 SCI 中的可能作用,以及 Snph 的一些可能的治疗方法。

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本文引用的文献

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TRAK adaptors regulate the recruitment and activation of dynein and kinesin in mitochondrial transport.TRAK 衔接蛋白调节线粒体运输中动力蛋白和驱动蛋白的募集和激活。
Nat Commun. 2023 Mar 13;14(1):1376. doi: 10.1038/s41467-023-36945-8.
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The interconnections between the microtubules and mitochondrial networks in cardiocerebrovascular diseases: Implications for therapy.心肌血管疾病中微管和线粒体网络的相互联系:对治疗的启示。
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Mitochondrial heterogeneity and homeostasis through the lens of a neuron.
通过神经元的视角看线粒体异质性和动态平衡。
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Magnesium-Encapsulated Injectable Hydrogel and 3D-Engineered Polycaprolactone Conduit Facilitate Peripheral Nerve Regeneration.镁胶囊化可注射水凝胶和 3D 工程聚己内酯导管促进周围神经再生。
Adv Sci (Weinh). 2022 Jul;9(21):e2202102. doi: 10.1002/advs.202202102. Epub 2022 Jun 2.
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Selective motor activation in organelle transport along axons.沿轴突的细胞器运输中的选择性运动激活。
Nat Rev Mol Cell Biol. 2022 Nov;23(11):699-714. doi: 10.1038/s41580-022-00491-w. Epub 2022 May 30.
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Programming axonal mitochondrial maintenance and bioenergetics in neurodegeneration and regeneration.调控轴突中线粒体的维持和生物能量在神经退行性变和再生中的作用。
Neuron. 2022 Jun 15;110(12):1899-1923. doi: 10.1016/j.neuron.2022.03.015. Epub 2022 Apr 16.
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8
SARM1 can be a potential therapeutic target for spinal cord injury.SARM1 可能成为治疗脊髓损伤的一个潜在靶点。
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Mitochondrial transport, partitioning, and quality control at the heart of cell proliferation and fate acquisition.线粒体运输、分割和质量控制是细胞增殖和命运获得的核心。
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