文献类型：期刊文献

英文题名：Induction mechanisms of autophagy and endoplasmic reticulum stress in intestinal ischemia-reperfusion injury, inflammatory bowel disease, and colorectal cancer

作者：Shi, Yan[1];Jiang, Bing[2];Zhao, Jingwen[3]

第一作者：Shi, Yan

通信作者：Zhao, JW[1]

机构：[1]Gansu Univ Tradit Chinese Med, Dept Basic Med, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Univ Tradit Chinese Med, Dept Integrated Chinese & Western Med, Lanzhou 730000, Gansu, Peoples R China;[3]Baoji Tradit Chinese Med Hosp, Dept Proctol, 43 Baofu Rd, Baoji 721001, Shanxi, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Baoji Tradit Chinese Med Hosp, Dept Proctol, 43 Baofu Rd, Baoji 721001, Shanxi, Peoples R China.

年份：2024

卷号：170

外文期刊名：BIOMEDICINE & PHARMACOTHERAPY

收录：;Scopus(收录号：2-s2.0-85179156107);WOS:【SCI-EXPANDED(收录号:WOS:001134934800001)】；

语种：英文

外文关键词：Autophagy; Endoplasmic reticulum stress; Intestinal ischemia-reperfusion injury; Inflammatory bowel disease; Colorectal cancer

摘要：In recent years, the incidence of intestinal ischemia-reperfusion injury (II/RI), inflammatory bowel disease (IBD), and colorectal cancer (CRC) has been gradually increasing, posing significant threats to human health. Autophagy and endoplasmic reticulum stress (ERS) play important roles in II/RI. Damage caused by ischemia and cellular stress can activate ERS, which in turn initiates autophagy to clear damaged organelles and abnormal proteins, thereby alleviating ERS and maintaining the intestinal environment. In IBD, chronic inflammation damages intestinal tissues and activates autophagy and ERS. Autophagy is initiated by upregulating ATG genes and downregulating factors that inhibit autophagy, thereby clearing abnormal proteins, damaged organelles, and bacteria. Simultaneously, persistent inflammatory stimulation can also trigger ERS, leading to protein imbalance and abnormal folding in the ER lumen. The activation of ERS can maintain cellular homeostasis by initiating the autophagy process, thereby reducing inflammatory responses and cell apoptosis in the intestine. In CRC, excessive cell proliferation and protein synthesis lead to increased ERS. The activation of ERS, regulated by signaling pathways such as IRE1 alpha and PERK, can initiate autophagy to clear abnormal proteins and damaged organelles, thereby reducing the negative effects of ERS. It can be seen that autophagy and ERS play a crucial regulatory role in the development of intestinal diseases. Therefore, the progress in targeted therapy for intestinal diseases based on autophagy and ERS provides novel strategies for managing intestinal diseases. In this paper, we review the advances in regulation of autophagy and ERS in intestinal diseases, emphasizing the potential molecular mechanisms for therapeutic applications.