Schwab Martin E, Strittmatter Stephen M
Brain Research Institute, University of Zurich, Winterthurerstr.190, Zurich CH-8057, Switzerland.
Department of Neurology, and Interdepartmental Program in Cellular Neuroscience, Neurodegeneration, and Repair (CNNR), Yale University School of Medicine, BCMM 436, 295 Congress Avenue, New Haven, CT 06510, USA.
Curr Opin Neurobiol. 2014 Aug;27:53-60. doi: 10.1016/j.conb.2014.02.011. Epub 2014 Mar 12.
The expression of Nogo-A and the receptor NgR1 limits the recovery of adult mammals from central nervous system injury. Multiple studies have demonstrated efficacy from targeting this pathway for functional recovery and neural repair after spinal cord trauma, ischemic stroke, optic nerve injury and models of multiple sclerosis. Recent molecular studies have added S1PR2 as a receptor for the amino terminal domain of Nogo-A, and have demonstrated shared components for Nogo-A and CSPG signaling as well as novel Nogo antagonists. It has been recognized that neural repair involves plasticity, sprouting and regeneration. A physiologic role for Nogo-A and NgR1 has been documented in the restriction of experience-dependent plasticity with maturity, and the stability of synaptic, dendritic and axonal anatomy.
Nogo-A及受体NgR1的表达限制成年哺乳动物中枢神经系统损伤后的恢复。多项研究已证明，针对该通路在脊髓损伤、缺血性中风、视神经损伤及多发性硬化症模型后实现功能恢复和神经修复具有疗效。最近的分子研究已将S1PR2添加为Nogo-A氨基末端结构域的受体，并证明了Nogo-A和硫酸软骨素蛋白聚糖（CSPG）信号传导的共同成分以及新型Nogo拮抗剂。人们已经认识到神经修复涉及可塑性、发芽和再生。Nogo-A和NgR1在限制成熟过程中依赖经验的可塑性以及突触、树突和轴突解剖结构的稳定性方面的生理作用已得到证实。
