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多发性硬化症中的少突胶质细胞发育与再生疗法

Oligodendrocyte Development and Regenerative Therapeutics in Multiple Sclerosis.

作者信息

Gacem Nadjet, Nait-Oumesmar Brahim

机构信息

Institut du Cerveau-Paris Brain Institute-ICM, Inserm, CNRS, AP-HP, Hôpital de la Pitié Salpêtrière, Sorbonne Université, 75013 Paris, France.

出版信息

Life (Basel). 2021 Apr 9;11(4):327. doi: 10.3390/life11040327.

Abstract

Myelination by oligodendrocytes (OLs) is an important biological process essential for central nervous system (CNS) development and functions. Oligodendroglial lineage cells undergo several morphological and molecular changes at different stages of their lineage progression into myelinating OLs. The transition steps of the oligodendrocyte progenitor cells (OPCs) to myelinating oligodendrocytes are defined by a specific pattern of regulated gene expression, which is under the control of coordinated signaling pathways. Any abnormal development, loss or failure of oligodendrocytes to myelinate axons can lead to several neurodegenerative diseases like multiple sclerosis (MS). MS is characterized by inflammation and demyelination, and current treatments target only the immune component of the disease, but have little impact on remyelination. Recently, several pharmacological compounds enhancing remyelination have been identified and some of them are in clinical trials. Here, we will review the current knowledge on oligodendrocyte differentiation, myelination and remyelination. We will focus on MS as a pathological condition, the most common chronic inflammatory demyelinating disease of the CNS in young adults.

摘要

少突胶质细胞(OLs)髓鞘形成是中枢神经系统(CNS)发育和功能所必需的重要生物学过程。少突胶质谱系细胞在其谱系进展为髓鞘形成性OLs的不同阶段经历了几种形态和分子变化。少突胶质前体细胞(OPCs)向髓鞘形成性少突胶质细胞的转变步骤由特定的调控基因表达模式定义,该模式受协调信号通路的控制。少突胶质细胞的任何异常发育、丢失或轴突髓鞘形成失败都可能导致多种神经退行性疾病,如多发性硬化症(MS)。MS的特征是炎症和脱髓鞘,目前的治疗仅针对该疾病的免疫成分,但对髓鞘再生影响甚微。最近,已经鉴定出几种增强髓鞘再生的药理化合物,其中一些正在进行临床试验。在这里,我们将综述关于少突胶质细胞分化、髓鞘形成和髓鞘再生的当前知识。我们将重点关注MS这种病理状况,它是年轻成年人中最常见的慢性炎症性脱髓鞘疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52b7/8069894/b06c418847aa/life-11-00327-g001.jpg

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