放射性脊髓病:一个老问题的新视角。

C Nieder, F Ataman, R E Price, K K Ang
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引用次数: 24

摘要

本文讨论了改变放射性脊髓病发病机制的基础研究的最新进展,并总结了脱髓鞘疾病的发育神经生物学和临床前研究的现有数据。这些研究对少突胶质细胞发育、细胞间信号通路和髓鞘形成过程产生了有趣的见解。目前的研究结果表明,在成人中枢神经系统(CNS)中,给予细胞因子作为血小板源性生长因子和碱性成纤维细胞生长因子可以增加少突胶质细胞祖细胞的增殖,增强其分化,上调髓磷脂成分的合成,促进髓磷脂再生。其他化合物也可能能够调节导致脊髓病的致病过程的进展。此外,还讨论了几种可能的生物预防或治疗策略,例如刺激内源性细胞再生和胶质细胞移植。合理设计动物实验,进一步阐明辐射致中枢神经系统损伤的发病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Radiation myelopathy: new perspective on an old problem.

This article discusses recent advances in basic research that alter the view of the pathogenesis of radiation myelopathy and summarizes the available data from developmental neurobiology and preclinical studies on demyelinating diseases. These studies have produced interesting insights into oligodendrocyte development, intercellular signaling pathways, and myelination processes. Current findings suggest that administration of cytokines as platelet-derived growth factor and basic fibroblast growth factor could increase proliferation of oligodendrocyte progenitors, enhance their differentiation, up-regulate synthesis of myelin constituents, and promote myelin regeneration in the adult central nervous system (CNS). Other compounds might also be able to modulate the progression of pathogenic processes that lead to myelopathy. In addition, several possible biological prevention or treatment strategies, for example stimulation of endogenous cellular regeneration and glial cell transplantation, are discussed. Rationally designed animal experiments pursuing such strategies could further elucidate the pathogenesis of radiation-induced CNS damage.

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