Regulation of remyelination in multiple sclerosis

被引:67
作者
Hanafy, Khalid A. [1 ]
Sloane, Jacob A. [1 ]
机构
[1] Beth Israel Deaconess Med Ctr, Dept Neurol, Ctr Life Sci, Boston, MA 02215 USA
关键词
Remyelination; Oligodendrocytes; Hyaluronan; Wnt; Notch1; Retinoid X receptor; OLIGODENDROCYTE PRECURSOR CELLS; CENTRAL-NERVOUS-SYSTEM; TRANSCRIPTION FACTOR-1 MYT1; ACTIVATED RECEPTOR-GAMMA; TOLL-LIKE RECEPTORS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; CNS REMYELINATION; PROGENITOR CELLS; ZINC-FINGER; SPINAL-CORD;
D O I
10.1016/j.febslet.2011.03.048
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Multiple sclerosis is a common demyelinating disease that worsens over the course of disease, a significant problem in clinical management. Disability in MS is significantly promoted by poor repair and remyelination of lesions. Both oligodendrocyte recruitment and maturation defects are seen as major causes of poor remyelination in MS. The mechanisms behind impaired remyelination in animal models include involvement of the Notch1, wnt, and hyaluronan/TLR2 pathways. RXR/PPAR signaling has also more recently been identified as an important regulator of remyelination. The local inflammatory milieu also appears to play critical and conflicting roles in promotion and inhibition of remyelination in MS. Understanding the forces regulating remyelination in MS represents an exciting and important initial step towards developing therapeutics targeting chronic disability in MS. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:3821 / 3828
页数:8
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