摘要
哺乳动物视神经损伤后不能成功再生,除了视网膜神经节细胞再生能力低下外,与中枢神经系统中存在抑制微环境密切相关。少突胶质细胞产生的髓鞘相关抑制分子是构成这种抑制微环境的重要成分。目前已经鉴定的抑制分子主要有 Nogo、髓磷脂相关糖蛋白及少突胶质细胞髓磷脂糖蛋白,他们通过同一受体复合体转导抑制信号。通过阻滞抑制分子及其受体或改变神经元的内在状态,可以克服抑制分子的抑制作用,促进视网膜神经节细胞轴索再生,为人类视神经损伤修复带来希望。
The failure of axonal regeneration after optic nerve injury in mammals is closely related to nonpermissive microenviroment in central nervous system as well as to the low regenerative ability of retinal ganglion cells. Myelin associated inhibitors produced by oligodendrocytes are major elements of this nonpermissive microenvironment. Three major inhibitors, Nogo, myelin-associated glycoprotein and oligodendrocyte myelin glycoprotein, have been identified, which lead to signal inhibition through the same receptor complex. Blocking the inhibitors and their receptors or changing the intrinsic state of the neuron to overcome the inhibition may promote retinal ganglion cell axonal regeneration after optic nerve injury, which bring a hope to solve the problem of repair of injured optic nerve.
出处
《中华眼科杂志》
CAS
CSCD
北大核心
2006年第9期854-858,共5页
Chinese Journal of Ophthalmology
基金
国家自然科学基金(30271333)
关键词
抗原
表面
髓磷脂相关糖蛋白
视神经损伤
神经再生
Antigens, surface
Myelin-associated glycoprotein
Optic nerve injuries
Nerve regeneration