Armstrong Regina C
Uniformed Services University of the Health Sciences, Department of Anatomy, Physiology & Genetics, 4301 Jones Bridge Rd, Bethesda, MD 20814-4799, USA, Tel.: +1 301 295 3205; ;
Future Neurol. 2007 Nov;2(6):689-697. doi: 10.2217/14796708.2.6.689.
Remyelination facilitates recovery of saltatory conduction along demyelinated axons and may help prevent axon damage in patients with demyelinating diseases, such as multiple sclerosis. The extent of remyelination in multiple sclerosis lesions varies dramatically, indicating a capacity for repair that is not fulfilled in lesions with poor remyelination. In experimental models of demyelinating disease, remyelination is limited by chronic disease that depletes the oligodendrocyte progenitor (OP) population, inhibits OP differentiation into remyelinating oligodendrocytes and/or perturbs cell survival in the lesion environment. Manipulating the activity of growth factor signaling pathways significantly improves the ability of endogenous OP cells to accomplish extensive remyelination. Specifically, growth factors have been identified that can regulate OP proliferation, differentiation and survival in demyelinated lesions. Therefore, growth factors may be key signals for strategies to improve conditions with poor remyelination.
髓鞘再生有助于脱髓鞘轴突的跳跃式传导恢复,并可能有助于预防脱髓鞘疾病(如多发性硬化症)患者的轴突损伤。多发性硬化症病变中的髓鞘再生程度差异很大,这表明在髓鞘再生不良的病变中,修复能力未得到充分发挥。在脱髓鞘疾病的实验模型中,慢性疾病会消耗少突胶质前体细胞(OP)群体,抑制OP分化为髓鞘再生少突胶质细胞和/或扰乱病变环境中的细胞存活,从而限制了髓鞘再生。操纵生长因子信号通路的活性可显著提高内源性OP细胞进行广泛髓鞘再生的能力。具体而言,已鉴定出可调节脱髓鞘病变中OP增殖、分化和存活的生长因子。因此,生长因子可能是改善髓鞘再生不良状况策略的关键信号。