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脊髓损伤再髓鞘化:治疗途径

Spinal Cord Injury Remyelination: Pathways to Therapies.

作者信息

Kaniuk Julia K, Kumar Divy, Tennyson Joshua, Hurka Kaitlyn L, Margolis Alexander, Bucaloiu Andrei, Selner Ashley, Ahuja Christopher S

机构信息

Feinberg School of Medicine, Northwestern University, 240 E Huron Street, Suite 1-200, Chicago, IL 60611, USA.

Northwestern Medicine Department of Neurological Surgery, 676 N St Clair Street, Suite 2210, Chicago, IL 60611, USA.

出版信息

Int J Mol Sci. 2025 Jul 26;26(15):7249. doi: 10.3390/ijms26157249.

DOI:10.3390/ijms26157249
PMID:40806380
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12346836/
Abstract

Spinal cord injury (SCI) is a debilitating condition that results from a culmination of acute and chronic damage to neural tissue, specifically the myelin sheath, thus impacting neurons' abilities to synergistically perform their physiological roles. This review explores the molecular underpinnings of myelination, demyelination, and remyelination, emphasizing the role of oligodendrocyte progenitor cells (OPCs), astrocytes, and microglia in physiological, and pathophysiological, healing. Furthermore, we link these processes with emerging therapeutic strategies currently under investigation in animal and human models, underscoring areas of translational medicine that remain underutilized. The goal of this review is to provide a framework for developing more advanced interventions to restore function and improve outcomes for individuals with SCI.

摘要

脊髓损伤(SCI)是一种使人衰弱的病症,它是由神经组织,特别是髓鞘的急性和慢性损伤累积所致,从而影响神经元协同发挥其生理作用的能力。本综述探讨了髓鞘形成、脱髓鞘和髓鞘再生的分子基础,强调了少突胶质前体细胞(OPC)、星形胶质细胞和小胶质细胞在生理及病理生理愈合过程中的作用。此外,我们将这些过程与目前在动物和人体模型中正在研究的新兴治疗策略联系起来,强调了转化医学中仍未得到充分利用的领域。本综述的目的是提供一个框架,以开发更先进的干预措施,为脊髓损伤患者恢复功能并改善预后。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02a0/12346836/1f963ffb2112/ijms-26-07249-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02a0/12346836/1f963ffb2112/ijms-26-07249-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02a0/12346836/1f963ffb2112/ijms-26-07249-g001.jpg

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本文引用的文献

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Factors Regulating Oligodendrocyte Progenitor Cell Migration: From Development to Remyelination.调节少突胶质前体细胞迁移的因素:从发育到髓鞘再生
Glia. 2025 Oct;73(10):1951-1966. doi: 10.1002/glia.70051. Epub 2025 Jun 13.
2
Low-Intensity Physical Exercise is Associated with Improved Myelination and Reduced Microglial Activation in a Cuprizone-Induced Demyelination Model.在铜螯合剂诱导的脱髓鞘模型中,低强度体育锻炼与髓鞘形成改善和小胶质细胞活化减少有关。
Neurochem Res. 2025 Jun 5;50(3):182. doi: 10.1007/s11064-025-04441-8.
3
The role of astrocyte-derived extracellular vesicles in cellular microenvironment remodeling after spinal cord injury: A study based on quantitative proteomics analysis.
星形胶质细胞衍生的细胞外囊泡在脊髓损伤后细胞微环境重塑中的作用:基于定量蛋白质组学分析的研究
Exp Neurol. 2025 Sep;391:115321. doi: 10.1016/j.expneurol.2025.115321. Epub 2025 May 27.
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Harnessing spinal circuit reorganization for targeted functional recovery after spinal cord injury.利用脊髓回路重组实现脊髓损伤后的靶向功能恢复。
Neurobiol Dis. 2025 Apr;207:106854. doi: 10.1016/j.nbd.2025.106854. Epub 2025 Feb 24.
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Mineral coated microparticles delivering Interleukin-4, Interleukin-10, and Interleukin-13 reduce inflammation and improve function after spinal cord injury in a rat.递送白细胞介素-4、白细胞介素-10和白细胞介素-13的矿物包被微粒可减轻大鼠脊髓损伤后的炎症并改善功能。
Exp Neurol. 2025 Apr;386:115179. doi: 10.1016/j.expneurol.2025.115179. Epub 2025 Feb 4.
6
Incomplete remyelination via therapeutically enhanced oligodendrogenesis is sufficient to recover visual cortical function.通过治疗性增强少突胶质细胞生成实现的不完全髓鞘再生足以恢复视觉皮层功能。
Nat Commun. 2025 Jan 16;16(1):732. doi: 10.1038/s41467-025-56092-6.
7
DNMT3b-mediated CpA methylation facilitates REST binding and gene silencing and exacerbates hippocampal demyelination in diabetic mice.DNMT3b介导的CpA甲基化促进REST结合和基因沉默,并加剧糖尿病小鼠的海马脱髓鞘。
J Biol Chem. 2025 Feb;301(2):108137. doi: 10.1016/j.jbc.2024.108137. Epub 2024 Dec 25.
8
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Lancet Neurol. 2025 Jan;24(1):42-53. doi: 10.1016/S1474-4422(24)00447-2.
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Nat Commun. 2024 Oct 9;15(1):8570. doi: 10.1038/s41467-024-52444-w.