JNK信号通路的激活在帕金森病发病机制中的作用

被引：8

作者：

关榆根 ^{[1
]}

张建鹏 ^{[2
]}

机构：

[1] 第二军医大学研究生管理大队学员九队

[2] 第二军医大学基础部生物化学与分子生物学教研室

来源：

生物技术通讯 | 2012年 / 23卷 / 06期

基金：

上海市自然科学基金;

关键词：

c-Jun氨基末端激酶; 帕金森病; 发病机制;

D O I：

暂无

中图分类号：

R742.5 [震颤麻痹综合征];

学科分类号：

1002 ;

摘要：

帕金森病是一种慢性中枢神经系统神经退行性疾病,主要以静止震颤、肌肉僵直和运动减少为临床症状,其确切病因尚不清楚。c-Jun氨基末端激酶(JNK)信号通路是MAPK通路的重要分支,在细胞周期、生长、凋亡和应激等生理和病理过程中发挥重要作用。研究显示,JNK信号通路与帕金森病的发生发展有很大关系,JNK信号通路的激活可导致线粒体复合体Ⅰ减少、细胞色素c释放、细胞内活性氧增加等一系列引起多巴胺能神经元功能异常,乃至细胞凋亡的反应的发生。我们通过总结DJ-1、乳胞素和猪毛菜酚等5种与JNK信号通路激活相关的内外源物质,简述JNK信号转导通路与PD的关系。

引用

页码：874 / 878

页数：5

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