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内质网应激诱导的糖尿病中的细胞凋亡和自身免疫

Endoplasmic reticulum stress-induced apoptosis and auto-immunity in diabetes.

作者信息

Lipson Kathryn L, Fonseca Sonya G, Urano Fumihiko

机构信息

Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, 01605-2324, USA.

出版信息

Curr Mol Med. 2006 Feb;6(1):71-7. doi: 10.2174/156652406775574613.

Abstract

Increasing evidence suggests that stress signaling pathways emanating from the endoplasmic reticulum (ER) are important to the pathogenesis of both type 1 and type 2 diabetes. Recent observations indicate that ER stress signaling participates in maintaining the ER homeostasis of pancreatic beta-cells. Either a high level of ER stress or defective ER stress signaling in beta-cells may cause an imbalance in ER homeostasis and lead to beta-cell apoptosis and autoimmune response. In addition, it has been suggested that ER stress attributes to insulin resistance in patients with type 2 diabetes. It is necessary to study the relationship between ER stress and diabetes in order to develop new therapeutic approaches to diabetes based on drugs that block the ER stress-mediated cell-death pathway and insulin resistance.

摘要

越来越多的证据表明,源自内质网(ER)的应激信号通路对1型和2型糖尿病的发病机制都很重要。最近的观察结果表明,内质网应激信号参与维持胰腺β细胞的内质网稳态。β细胞中高水平的内质网应激或有缺陷的内质网应激信号都可能导致内质网稳态失衡,进而导致β细胞凋亡和自身免疫反应。此外,有人提出内质网应激与2型糖尿病患者的胰岛素抵抗有关。研究内质网应激与糖尿病之间的关系,以便基于阻断内质网应激介导的细胞死亡途径和胰岛素抵抗的药物开发新的糖尿病治疗方法是很有必要的。

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