中枢神经损伤后TGF-β1信号通路对神经再生的影响  

The effect of TGF-β1 on neuroregeneration and scar formation after central nervous system injury

作　　者：张馨月 李洪鹏[2] 

机构地区：[1]大连医科大学,大连116044 [2]中国医科大学人体解剖学教研室,沈阳110122

出　　处：《解剖科学进展》2017年第6期653-655,657,共4页Progress of Anatomical Sciences

基　　金：国家自然科学基金(81171248)

摘　　要：中枢神经损伤后TGF-β1信号通路被激活,引起损伤周边的瘢痕组织的增生与形成,瘢痕组织包括损伤中心区的纤维瘢痕和损伤周边的胶质瘢痕。虽然在早期对修复血脑屏障起着重要的作用,但后期瘢痕组织的过度增生会产生大量的抑制神经再生的细胞外基质,如硫酸软骨素蛋白糖。因此,在损伤后期抑制TGF-β1信号的持续激活可能促进神经轴突的再生。从TGF-β1信号通路与瘢痕组织形成的相关性研究中枢神经损伤后的神经再生机制具有重要意义。TGF- beta1 signaling pathway was activated after the central nervous system （CNS） injury, and induced the scar hyperplasia and formation. The scar tissue includes the fibrous scar in the center of the lesion and the glial scar around the lesion site. Though the scar tissue plays an important role for repairing the blood brain barrier at the early stage after CNS injury, the excessive proliferation of the scar tissue will produce a great deal of extracellular matrix such as chondroitin sulfate proteoglycans impeding neuroregeneration in the late. Inhibition of sustainable activation of TGF- beta1 signaling pathway at the late would promote the axonal regeneration. The study of the relationship of TGF- beta1 signaling pathway and scar formation will have significant value to clarify the mechanism of neuroregeneration after CNS injury.

关 键 词：中枢神经损伤 抑制神经再生 信号通路 TGF 瘢痕组织形成 神经再生机制 过度增生 细胞外基质 

分 类 号：R741.02[医药卫生—神经病学与精神病学]