摘要
内质网应激是继死亡受体信号途径和线粒体途径之后新近发现的一条细胞凋亡通路,适度的应激可通过未折叠蛋白反应(UPR)产生细胞保护作用,但当应激过强或长时间不缓解时则会触发CHOP、ASK1/JNK及Caspases等通路诱导细胞凋亡。近年来研究发现内质网应激参与多种心血管疾病的发生发展,通过对相关通路的干预可以产生心肌细胞的保护作用,这有望成为防治心脏疾病的新靶点。
Endoplasmic reticulum stress is a newly discovered pathway of apoptosis,following the death receptor signaling and mitochondrial pathways.Moderate stress triggers the unfolded protein response(UPR) to rsstore the cell function.However,if the stress is severe and/or prolonged,the ER also initiates apoptotic signaling that includes CHOP,ASK1/JNK and caspases pathways.Recent studies have found that endoplasmic reticulum stress plays an important role in the development of various cardiovascular diseases.Also,extensive research has shown that it can bring about protective effects on myocardial cells through the intervention of the relevant pathways,which may provide us with new therapeutic targets for heart diseases.
出处
《生理科学进展》
CAS
CSCD
北大核心
2011年第6期419-422,共4页
Progress in Physiological Sciences
基金
国家科技部国际科技合作重大专项课题(2006DFB32210)
关键词
内质网应激
凋亡
心血管疾病
细胞保护
endoplasmic reticulum stress
apoptosis
cardiovascular disease
cell protection
