Regulation of MAPK pathway and autophagic flux by ROS promotes apoptosis during ER stress

• 作 者: Xiangxiyan;Sunliankun;
• 机 构: Department of Pathophysiology,Norman Bethune College of Medicine,Jilin University,Changchun,Jilin 13
• 出 处: 中国病理生理学会第十四届肿瘤专业委员会、第十五届免疫专业委员会联合学术会议
• 发表日期: 2014年期

　　As new targets for cancer therapy,endoplasmic reticulum (ER) stress and autophagy are closely linked,with evidence suggesting that ER stress can activate autophagy through UPR.Although generally thought as an adaptive response by clearing "garbages" accumulated in the lumen,autophagy activation during ER stress may also contribute to cell death when the stress is prolonged or too severe.To date,however,the exact mechanisms by which the proapoptotic outputs of autophagy and ER stress are integrated to select death cell fate are very poorly characterized.