c-Jun氨基端激酶通路、内质网应激、氧化应激与胰岛β细胞功能  

Effect of JNK pathway, endoplasmic reticulum stress and oxidative stress on pancreatic islet β cell function

作　　者：侯志强[1] 李宏亮[1] 李光伟[1] 

机构地区：[1]中日友好医院内分泌代谢病中心,北京100029

出　　处：《中华内分泌代谢杂志》2008年第3期348-350,共3页Chinese Journal of Endocrinology and Metabolism

摘　　要：尽管对2型糖尿病时胰岛β细胞功能受损及凋亡的具体机制目前尚不清楚，但研究发现糖尿病时诱导或加重的内质网应激及氧化应激可导致胰岛β细胞功能损伤，尤其是c—Jun氨基端激酶通路作为两者的共同通路在其中发挥着重要作用。Though the mechanisms involved in the induction of pancreatic islet β cell dysfunction and apoptosis under diabetes conditions are still not clear, previous studies have shown that triggered or aggravated endoplasmic reticulum stress and oxidative stress play essential roles in impairment of β cell functions, especially the JNK pathway which can be activated by both of them.

关 键 词：c—Jun氨基端激酶 内质网应激 氧化应激 胰岛Β细胞 

分 类 号：R587.1[医药卫生—内分泌] R743.31[医药卫生—内科学]