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促进轴突髓鞘形成以改善脊髓损伤的神经功能恢复。

Promoting axonal myelination for improving neurological recovery in spinal cord injury.

机构信息

Department of Orthopedics, Xinqiao Hospital, The Third Military Medical University, Chongqing, China.

出版信息

J Neurotrauma. 2009 Oct;26(10):1847-56. doi: 10.1089/neu.2008.0551.

Abstract

Spinal cord injury (SCI) remains a major challenge to neurological research. Progress in both basic and clinical research has shown that neurons and oligodendrocytes are equally susceptible to such injury. In injuries secondary to direct injury to the spinal cord, oligodendrocytes appear to be highly vulnerable to various harmful factors and eventually undergo apoptosis. Due to the loss of myelinating cells, axonal demyelination is likely to affect the neural function of surviving axons. Recently, improved understanding of the pathological changes ongoing in oligodendrocytes following injury has shown that the death of these cells plays a vital role in the demyelination of axons. Because the demise of oligodendrocytes and subsequent axonal demyelination impair the conductive capacity of surviving axons, it seems reasonable to expect that reducing oligodendrocyte death and improving axonal myelination holds potential for the treatment of SCI. In the clinical setting, such therapy may help these patients, including those with complete functional injury and those with white matter preservation. Accordingly, it appears reasonable that improving axonal myelination and the conductive capacity of surviving axons will be of great benefit in patients with mild to moderate injury of the spinal cord. We here present a review of the pathophysiology and mechanisms of oligodendrocyte death and axonal demyelination that follow injury to the spinal cord, and discuss the potential for treating them. Because cell transplantation has recently become a promising strategy for replacing lost oligodendrocytes and improving axonal myelination in SCI, we also discuss the significance of cell transplantation as a novel approach to treating SCI.

摘要

脊髓损伤 (SCI) 仍然是神经科学研究的主要挑战。基础和临床研究的进展表明,神经元和少突胶质细胞同样容易受到这种损伤。在继发于脊髓直接损伤的损伤中,少突胶质细胞似乎对各种有害因素高度敏感,最终会发生细胞凋亡。由于髓鞘形成细胞的丧失,轴突脱髓鞘很可能影响存活轴突的神经功能。最近,对损伤后少突胶质细胞发生的病理变化的深入了解表明,这些细胞的死亡在轴突脱髓鞘中起着至关重要的作用。由于少突胶质细胞的死亡和随后的轴突脱髓鞘损害了存活轴突的传导能力,因此,减少少突胶质细胞的死亡和改善轴突髓鞘化有望成为 SCI 的治疗方法。在临床环境中,这种治疗方法可能对这些患者有益,包括那些功能完全损伤和那些保留白质的患者。因此,改善轴突髓鞘化和存活轴突的传导能力似乎对脊髓损伤程度较轻和中等的患者有很大的好处。我们在这里综述了脊髓损伤后少突胶质细胞死亡和轴突脱髓鞘的病理生理学和机制,并讨论了治疗它们的可能性。由于细胞移植最近已成为替代丢失的少突胶质细胞和改善 SCI 中轴突髓鞘化的有前途的策略,我们还讨论了细胞移植作为治疗 SCI 的新方法的意义。

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