Endoplasmic reticulum stress in the intestinal epithelium and inflammatory bowel disease.
Endoplasmic reticulum stress in the intestinal epithelium and inflammatory bowel disease.
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肠上皮和炎症性肠病中的内质网应激。
DOI：
10.1016/j.smim.2009.01.001
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发表时间：
2009-06
影响因子：
7.8
通讯作者：
Blumberg RS
中科院分区：
文献类型：
--
作者：
Kaser A;Blumberg RS
内质网应激引起的未折叠蛋白反应是导致炎症性肠病（IBD）的一种新机制。在高度分泌的潘氏细胞中，以及在较小程度上，上皮内的杯状细胞中，适当的ER应激分辨率的受损可主要导致肠道炎症。不能管理ER应激可能不仅是肠道炎症的主要起源，如与IBD相关的XBP1基因多态性所例示的，而且当ER应激继发于炎症介质或微生物因子时，也是炎症的永久化因素。此外，ER应激途径可能与导致IBD的其他过程相互作用，特别是自噬。
The unfolded protein response as a consequence of endoplasmic reticulum (ER) stress has recently been implicated as a novel mechanism that may lead to inflammatory bowel disease (IBD). Impairment of proper ER stress resolution in highly secretory Paneth and, to a lesser extent, goblet cells within the epithelium can primarily lead to intestinal inflammation. An inability to manage ER stress may not only be a primary originator of intestinal inflammation as exemplified by genetic polymorphisms in XBP1 that are associated with IBD but also a perpetuator of inflammation when ER stress is induced secondarily to inflammatory mediators or microbial factors. Furthermore, ER stress pathways may interact with other processes that lead to IBD, notably autophagy.