少突胶质细胞代谢综述。

Q3 Neuroscience
Qi Han, Jin Cheng
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引用次数: 0

摘要

少突胶质细胞(OLs)表现出复杂的代谢相互作用,对神经元功能和中枢神经系统健康至关重要。本章分析OLs的代谢,特别是葡萄糖、脂质和氨基酸代谢,以及它们对髓磷脂合成、维持和中枢神经系统恢复能力的影响。ol通过糖酵解和戊糖磷酸途径利用葡萄糖作为能量,支持ATP的产生和抗氧化防御。脂质合成,包括胆固醇和鞘脂的产生,对于维持髓磷脂的完整性和快速信号传导至关重要。此外,氨基酸途径,如涉及谷氨酰胺和丝氨酸的途径,调节OL分化和髓鞘再生。ol还通过乳酸穿梭及其与盘状神经网络中的星形胶质细胞的相互作用为神经元提供代谢支持,确保持续的能量流动。OL代谢功能失调是脱髓鞘疾病(如多发性硬化症、神经退行性疾病和神经精神疾病)的基础,强调了靶向OL代谢以增强髓鞘再生和神经保护的治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
An Overview of Oligodendrocyte Metabolism.

Oligodendrocytes (OLs) exhibit complex metabolic interactions essential for neuronal function and CNS health. This chapter analyzes the metabolism of OLs, particularly glucose, lipid, and amino acid metabolism, and their impact on myelin synthesis, maintenance, and CNS resilience. OLs utilize glucose for energy through glycolysis and the pentose phosphate pathway, supporting ATP production and antioxidative defenses. Lipid synthesis, including cholesterol and sphingolipid production, is critical for maintaining myelin integrity and rapid signal conduction. Furthermore, amino acid pathways, such as those involving glutamine and serine, modulate OL differentiation and remyelination. OLs also provide metabolic support to neurons through lactate shuttling and their interactions with astrocytes in the Panglial network, ensuring sustained energy flow. Dysregulation of OL metabolic functions underlies demyelinating diseases, such as multiple sclerosis, neurodegenerative disorders, and neuropsychiatric conditions, highlighting the therapeutic potential of targeting OL metabolism to enhance remyelination and neuroprotection.

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来源期刊
Advances in neurobiology
Advances in neurobiology Neuroscience-Neurology
CiteScore
2.80
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0.00%
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