Department of Neurology, Beth Israel Deaconess Medical Center, Center for Life Sciences, Boston, MA 02215, United States.
FEBS Lett. 2011 Dec 1;585(23):3821-8. doi: 10.1016/j.febslet.2011.03.048. Epub 2011 Mar 30.
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.
多发性硬化症是一种常见的脱髓鞘疾病，其病情在病程中会逐渐恶化，这是临床管理中的一个重大问题。MS 患者的残疾程度与病变的不良修复和再髓鞘密切相关。少突胶质细胞的募集和成熟缺陷被认为是 MS 中再髓鞘不良的主要原因。在动物模型中，再髓鞘障碍的机制包括 Notch1、wnt 和透明质酸/TLR2 途径的参与。最近，RXR/PPAR 信号也被确定为再髓鞘的重要调节因子。局部炎症环境在 MS 中的再髓鞘促进和抑制中似乎也起着关键和冲突的作用。了解调节 MS 中再髓鞘的因素是朝着开发治疗 MS 慢性残疾的治疗方法迈出的令人兴奋且重要的第一步。
