文献类型：期刊文献

英文题名：The role of endoplasmic reticulum stress in type 2 diabetes mellitus mechanisms and impact on islet function

作者：He, Zhaxicao[1];Liu, Qian[1];Wang, Yan[1];Zhao, Bing[1];Zhang, Lumei[1];Yang, Xia[2];Wang, Zhigang[1,2]

第一作者：He, Zhaxicao

机构：[1]Gansu Univ Chinese Med, Lanzhou, Peoples R China;[2]Tianshui Hosp Tradit Chinese Med, Tianshui, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]Gansu University of Chinese Medicine, Lanzhou, China|[10735]甘肃中医药大学;

年份：2025

卷号：13

期号：3

外文期刊名：PEERJ

收录：;Scopus(收录号：2-s2.0-105001688346);WOS:【SCI-EXPANDED(收录号:WOS:001477689200001)】；

基金：This work was supported by the Natural Science Foundation of Gansu Province (No.25JRRE013) and the Subject of Gansu Provincial Administration of Chinese Medicine(No. GZKZ-2024-39). The funders had no role in study design, data collection andanalysis, decision to publish, or preparation of the manuscript.

语种：英文

外文关键词：Diabetes; Endoplasmic reticulum stress; Pancreatic cell; Unfolded protein response; Therapeutic strategies; Islet cell

摘要：Type 2 diabetes mellitus (T2DM) is a globally prevalent metabolic disorder characterized by insulin resistance and dysfunction of islet cells. Endoplasmic reticulum (ER) stress plays a crucial role in the pathogenesis and progression of T2DM, especially in the function and survival of beta-cells. beta-cells are particularly sensitive to ER stress because they require substantial insulin synthesis and secretion energy. In the early stages of T2DM, the increased demand for insulin exacerbates beta-cell ER stress. Although the unfolded protein response (UPR) can temporarily alleviate this stress, prolonged or excessive stress leads to pancreatic cell dysfunction and apoptosis, resulting in insufficient insulin secretion. This review explores the mechanisms of ER stress in T2DM, particularly its impact on islet cells. We discuss how ER stress activates UPR signaling pathways to regulate protein folding and degradation, but when stress becomes excessive, these pathways may contribute to beta-cell death. A deeper understanding of how ER stress impacts islet cells could lead to the development of novel T2DM treatment strategies aimed at improving islet function and slowing disease progression.