摘要
内质网是蛋白质合成、修饰以及折叠的重要场所。内质网内未折叠蛋白堆积,钙离子失稳等可触发内质网应激,通过非折叠蛋白应答纠正这些异常变化。过度的内质网应激或内质网应激机制失常将导致细胞损害和死亡。近年来的研究发现阿尔茨海默病的神经系统损害与内质网应激异常有关。深入研究内质网应激将为进一步探索阿尔茨海默病发病机制和防治基础提供新的方向。
The endoplasmic reticulum （ER） is an important subcelluar organelle for the synthesis, posttranslational modification, and proper folding of protein. In some conditions, such as accumulation of unfolded protein or disruption of calcium in ER, ER stress is provoked. Normal cells respond to ER stress by activation of the unfolded protein response, to prevent protein misfolding, degrade misfolded protein and facilitate protein proper folding in ER. However, excessive or aberrant ER stress results in cell injury or death. Recent evidence indicates that neurodegenerative disorders in Alzheimer＇s disease are associated to aberrant ER stress. Further resolution of the molecular relationship between ER stress and neurodegeneration will provide novel insights into the mechanisms of AD pathology, and lead to new therapeutic targets for AD.
出处
《细胞生物学杂志》
CSCD
2006年第4期518-522,共5页
Chinese Journal of Cell Biology
关键词
内质网应激
非折叠蛋白反应
凋亡
阿尔茨海默病
早老蛋白
endoplasmic reticulum stress
unfolded protein response
apoptosis
Alzheimer＇s disease
presenilin
