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多发性硬化是一类中枢神经系统炎症性脱髓鞘疾病,其发病原因目前尚未明确。深入地研究该疾病的发生发展机制将为临床预防及治疗提供更有效的帮助。髓鞘是中枢神经系统重要的生理结构,主要发挥保护轴突和加速神经冲动传导的作用。在成年中枢神经系统,髓鞘损伤后可以由少突胶质前体细胞经增殖、迁移和分化而重新形成,即髓鞘再生。然而,在慢性多发性硬化症患者的病灶中,由于少突胶质前体细胞分化障碍,导致髓鞘再生减弱,进而造成轴突损伤和神经元丢失,发生不可逆的神经功能障碍,是进展型多发性硬化发生的重要原因。因此,研究进展型多发性硬化患者病灶中少突胶质前体细胞的分化障碍及其相关信号机制对于临床治疗和药物开发具有重要意义。本综述将着眼于少突胶质前体细胞的分化调控机制,分析其在进展型多发性硬化病理发生中的作用和意义,并讨论了相关的潜在治疗靶点。
Multiple sclerosis is a type of central nervous system inflammatory demyelinating disease, the etiology of which is not yet clear. In-depth study of the occurrence and development of the disease mechanism for clinical prevention and treatment to provide more effective help. Myelin is an important physiological structure of the central nervous system, mainly to protect the axon and accelerate nerve impulse conduction. In adult central nervous system, myelin damage can be regenerated by the proliferation, migration and differentiation of oligodendrocyte precursor cells, ie remyelination. However, in patients with chronic multiple sclerosis, irreversible neurological dysfunction is a progressive type of disease due to a disorder of differentiation of oligodendrocyte precursor cells, which leads to a decrease in remyelination and subsequent axonal injury and neuronal loss Multiple sclerosis occurs an important reason. Therefore, to study the differentiation disorders of oligodendrocyte precursor cells and their related signaling mechanisms in patients with progressive multiple sclerosis is of great significance for clinical treatment and drug development. This review will focus on the regulation of oligodendrocyte precursor cell differentiation and analysis of its role in the pathogenesis of progressive multiple sclerosis and its significance, and discusses the potential therapeutic targets.