| 摘要: |
| 内质网应激是细胞对于内源性应激的一种适应性反应,由未折叠蛋白所诱导,其机制被称为未折叠蛋白反应(UPR).哺乳动物UPR包含3个经典的分支通路,分别以胰腺内质网激酶(PERK)、需肌醇跨膜激酶/核酸内切酶1(IRE1)和活化转录因子6(ATF6)作为近端效应物,能够促进蛋白质折叠和转运,停止蛋白质的翻译合成,降解清除错误蛋白,并可启动凋亡程序诱导不能修复错误蛋白的细胞凋亡,从而维持内环境与组织细胞功能的稳态.支气管上皮内含多种蛋白质合成分泌旺盛的细胞类型,本身易出现内质网应激;支气管哮喘时,气道炎症状态等因素的存在被认为可以诱发UPR,并与气道炎症反应互为因果,交互作用.目前的研究认为,在支气管哮喘发病中,气道上皮细胞的钙稳态失调、透明质酸与黏蛋白的异常分泌、细胞因子对炎细胞的募集作用以及免疫调节状态的异常等环节与内质网应激存在密切的关系.本文即对内质网应激与哮喘的相关研究作一综述. |
| 关键词: 内质网应激 哮喘 未折叠蛋白反应 |
| DOI：10.3724/SP.J.1008.2015.00074 |
| 投稿时间：2014-05-11修订日期：2014-08-25 |
| 基金项目:国家自然科学基金(81000006),上海市浦江人才计划(14PJ1411000). |
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| Endoplasmic reticulum stress and bronchial asthma |
| WANG Ying△,XIONG Ye△,SHANG Yan*,LI Qiang,BAI Chong |
(Department of Respiratory Medicine, Changhai Hospital, Second Military Medical University, Shanghai 200433, China
△Co-first authors.
*Corresponding author) |
| Abstract: |
| The endoplasmic reticulum stress (ERS) response is induced by misfolded proteins via the unfolded-protein response (UPR),allowing cells to deal with endogenous stress through arresting of protein translation,promoting peptide folding,degeneration of unfolded or misshapen proteins,and cell apoptosis.Pancreatic endoplasmic reticulum kinase (PERK),inositol-requiring transmembrane kinase/endonuclease 1 (IRE1) and activating transcription factor 6 (ATF6) are the three proximal effectors of the UPR in mammalian cells.Airway epithelial cells consist of many cell types with prosperous cell growth and numerous secretion,making those cells more liable to have ERS.Recent studies have revealed the role of ERS in the pathogenesis of bronchial asthma,which involves imbalance of calcium homeostasis,abnormal secretion of hyaluronic acid and mucin,and the abnormal recruitment and infiltration of inflammatory cells.This article summarizes the correlation of ERS with asthma. |
| Key words: endoplasmic reticulum stress asthma unfolded protein response |
