中文摘要：

多种生理或病理条件会引起未折叠蛋白或错误折叠蛋白在内质网的聚集,损伤内质网的正常生理功能,此现象称为内质网应激（endoplasmic reticulum stress,ERS）。ERS时,许多分子伴侣蛋白,如：葡萄糖调节蛋白、钙联蛋白以及钙网蛋白等的表达出现上调,参与调控ERS过程,甚至启动caspase 12、CHOP/GADDl53等促凋亡因子表达和活化。目前,对一些疾病,如：酒精性肝病和阿尔兹海默病等的研究表明,疾病的病理机制中可见内质网分子伴侣的表达变化,提示疾病的发生与ERS可能有相关性。本文旨在对与ERS相关的分子伴侣的基本结构和调控过程以及相关疾病的病理机制进行综述。

英文摘要：

Many physiological or pathological conditions can cause the collection of unfolded proteins or wrongfolded proteins in endoplasmic reticulum, and cause the injury of endoplasmic reticulum’s physiological functions. This phenomenon is called endoplasmic reticulum stress（ERS）. During ERS, many molecular chaperones have higher expression,such as glucose-regulated proteins（GRPs）, Calnexin（CNX） and calreticulin（CRT）. The molecular chaperones overexpressed in some diseases such as alcoholic liver disease and Alzheimer’s disease. This article aims to review basic structures and controlling processes of molecular chaperones participating in ERS and pathological mechanism of related diseases.