JNK信号通路与胰岛β细胞凋亡

JNK Signaling Pathway and Islet Beta Cell Apoptosis

关键词:  c-Jun氨基端激酶  凋亡  活性氧  线粒体凋亡  内质网应激

Key words:  c-Jun N-terminal kinase  apoptosis  reactive oxygen species  mitochondrial apoptosis  endoplasmic reticulum stress

摘要:

c-Jun氨基端激酶（c-Jun N-terminal kinase，JNK）信号通路是近几年发现的与细胞凋亡机制、应激反应以及糖尿病发生与发展关系密切的通路之一，其生物学效应对胰岛β细胞的调节至关重要。根据刺激源的不同，JNK会介导3条凋亡通路的激活，包括死亡受体通路、线粒体凋亡通路以及内质网应激通路，各通路之间以某个因子或刺激源而产生串扰关系。活性氧作为应激源可以激活JNK信号通路，从而激活相关凋亡通路。因此，对JNK信号通路的各个节点进行调控，极有可能减少胰岛β细胞凋亡数量，保护胰腺组织完整性，降低糖尿病及并发症的风险。

Abstract:

c-Jun N-terminal kinase (JNK) signaling pathway is found in recent years and is one of the pathways of closely related to mechanism of cell apoptosis, shock response as well as the occurrence and development of diabetes, which its biological effect is important for the regulation of islet beta cells. According to different stimuli, the JNK is mediated three activation of apoptotic pathways, including death receptor pathway, mitochondrial apoptosis pathway and endoplasmic reticulum stress activation pathway, between various pathways to a factor or stimuli and produce crosstalk relationship. Reactive oxygen species (ROS) as a source of stress can activates JNK signaling pathway, so then excited apoptosis pathway. Therefore, to adjust and control on every node of the JNK signaling pathway, which are likely to reduce the number of islet beta cell apoptosis, protect pancreatic tissue integrity, reduce the risk of diabetes and complications.