c-Jun氨基末端激酶在脑缺血再灌注损伤中的作用  

Role of c-Jun N-terminal kinase in brain ischemia reperfusion injury

作　　者：刘莎莎[1] 高维娟[1] 

机构地区：[1]承德医学院病理生理学教研室,河北承德067000

出　　处：《中国病理生理杂志》2011年第3期607-610,共4页Chinese Journal of Pathophysiology

基　　金：教育部新世纪优秀人才支持计划资助项目(No.NCET-06-0258);河北省自然科学基金重点资助项目(No.C2006000865)

摘　　要：在生物体内,丝裂原活化蛋白激酶（mitogen-activated protein kinase,MAPK）是信号从细胞表面转导至细胞核内部的重要传递者,是一类丝/苏氨酸残基的蛋白激酶。目前在真核生物细胞中,已明确了4条MAPK信号转导通路[1],c-Jun N-terminal kinase（JNK）,a member of the mitogen-activated protein kinase family,is activated in response to a number of extracellular stimuli,including inflammatory cytokines,UV irradiation and ischaemia.A large amount of evidence supports the key role for JNK signaling in stress-induced apoptosis.Recent studies suggest that JNK signaling pathway is involved in neuron death by controlling both the death receptor pathway and the mitochondrial-dependent pathway after transient ischemia.The role of the JNK signaling pathway in brain ischemia reperfusion injury is overviewed in this article.

关 键 词：JNK通路 信号转导 脑缺血再灌注 细胞凋亡 

分 类 号：R363[医药卫生—病理学]