内质网应激与肝细胞凋亡
内质网应激;肝细胞凋亡;未折叠蛋白反应,吴涛,季光,郑培永,柳涛,通讯作者:,Endoplasmicreticulumstressandhepaticapoptosis,TaoWu,GuangJi,Pei-YongZheng,TaoLiu,Supportedby:
 |
| 第7页 |
 |
| 第1页 |
参见附件(1068KB，9页)。
吴涛, 季光, 郑培永, 柳涛, 上海中医药大学附属龙华医院消化内科 上海中医药大学脾胃病研究所 上海市 200032
国家自然科学基金资助项目, No. 30572380
通讯作者: 季光, 200032, 上海市宛平南路725号, 上海中医药大学附属龙华医院消化内科, 上海中医药大学脾胃病研究所. jiliver@vip.sina.com
电话: 021-64286261 传真: 021-64286261
收稿日期: 2007-06-16 修回日期: 2007-08-10
Endoplasmic reticulum stress and hepatic apoptosis
Tao Wu, Guang Ji, Pei-Yong Zheng, Tao Liu
Tao Wu, Guang Ji, Pei-Yong Zheng, Tao Liu,Department of Gastroenterology, Research Institute of Spleen and Stomach Diseases, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China
Supported by:National Natural Science Foundation of China, No. 30572380
Correspondence to:Guang Ji, Department of Gastroenterology, Research Institute of Spleen and Stomach Diseases, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, 725 Wanping South Road, Shanghai 200032, China. jiliver@vip.sina.com
Received:2007-06-16 Revised:2007-08-10
Abstract
Endoplasmic reticulum (ER) is an important organelle of eukaryotic cells. There are many reasons for the accumulation of misfolded and unfolded proteins in the ER, which affect the balance of Ca2+. Such phenomena are called ERS. Apoptosis, programmed cell death, is an active method of cell death controlled by the extracellular microenvironment and intracellular gene regulation. It is an important mechanism by which the body removes no-longer-needed cells and heterocysts, thus ensuring normal development and maintaining the normal physiological processes of the organism. Hepatic apoptosis can cause liver injury and disease, and is considered to be mainly mediated by two signaling pathways: the death acceptor and the mitochondrial pathways of cell death. However, recent research has demonstrated that ERS also mediates hepatic apoptosis. The mechanism of hepatic apoptosis mediated by ERS is discussed ......
您现在查看是摘要介绍页，详见PDF附件(1068KB，9页)。