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少突胶质细胞保护、血脑屏障破坏和炎症对髓鞘修复的重要性。

Importance of oligodendrocyte protection, BBB breakdown and inflammation for remyelination.

机构信息

Departments of Neurology and Immunology, Mayo Clinic College of Medicine, 200 First Street, SW, Rochester, MN 55905, USA.

出版信息

Expert Rev Neurother. 2010 Mar;10(3):441-57. doi: 10.1586/ern.10.13.

Abstract

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the CNS. A better understanding of why remyelination fails in MS is necessary to improve remyelination strategies. Remyelination is mediated by oligodendrocyte precursor cells (OPCs), which are widely distributed throughout the adult CNS. However, it is still unclear whether OPCs detectable in MS lesions survive the inflammatory response but are unable to myelinate or whether OPC and oligodendrocyte death is primarily responsible for remyelination failure and detectable OPCs enter demyelinated areas from adjacent tissue as the lesion evolves. Remyelination strategies should, therefore, focus on stimulation of differentiation or prevention of apoptosis, as well as establishment of a supportive environment for OPC-mediated remyelination, which may be especially important in chronically demyelinated lesions.

摘要

多发性硬化症(MS)是一种中枢神经系统的慢性炎症性脱髓鞘疾病。为了改善髓鞘再生策略,有必要更好地了解为何 MS 中的髓鞘再生会失败。髓鞘再生由少突胶质前体细胞(OPC)介导,OPC 广泛分布于成年中枢神经系统中。然而,目前尚不清楚在 MS 病变中检测到的 OPC 是否在炎症反应中存活但无法进行髓鞘形成,还是 OPC 和少突胶质细胞的死亡是导致髓鞘再生失败的主要原因,以及随着病变的发展,OPC 是否从相邻组织进入脱髓鞘区域。因此,髓鞘再生策略应侧重于刺激分化或预防细胞凋亡,以及为 OPC 介导的髓鞘再生建立支持性环境,这在慢性脱髓鞘病变中可能尤为重要。

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