Mechanisms underlying remyelination with special focus on demyelination models of multiple sclerosis.
10.3785/j.issn.1008-9292.2020.08.12
- Author:
Shuangshuang ZHENG
1
;
Jingwei ZHAO
1
Author Information
1. Department of Human Anatomy, Histology and Embryology, System Medicine Research Center, Zhejiang University School of Medicine, Hangzhou 310058, China.
- Publication Type:Journal Article
- Keywords:
Multiple sclerosis;
Oligodendrocyte progenitor cells;
Remyelination
- From:
Journal of Zhejiang University. Medical sciences
2020;49(4):524-530
- CountryChina
- Language:Chinese
-
Abstract:
Failure to remyelinate and rewrap the demyelinated axons has been revealed as the major hurdle for treatment of multiple sclerosis (MS), and the bottleneck is the inability of oligodendrocyte progenitor cell (OPC) to differentiate into mature oligodendrocyte. Remyelination is a spontaneous regenerative process, which includes activation, migration and differentiation of OPC, and is believed to protect the axon and further halt neurodegeneration. In recent years, studies have identified many potential drug targets for efficiently promoting OPC differentiation in demyelination models, such as metformin, clemostine, and drug targets as myelin transcription factor 1-like protein (Myt1L), N-methyl-D-aspartic acid (NMDA) receptor, connexin 43 (Cx43), G protein coupled receptor 17 (GPR17), κ opioid receptor (KOR), sterol 14α-demethylase (CYP51), Δ14-sterol reductase (TM7SF2), emopamil-binding protein (EBP). This review summarizes the recent progress on the mechanisms underlying the activation, migration and differentiation of OPC in remyelination with special focus on studies using demyelination models of MS, which may provide insights of further exploring new therapeutic strategies for MS.
