Endoplasmic reticulum stress: implications for inflammatory bowel disease pathogenesis.
Endoplasmic reticulum stress: implications for inflammatory bowel disease pathogenesis.
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DOI：
10.1097/mog.0b013e32833a9ff1
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发表时间：
2010-07
影响因子：
2.5
通讯作者：
Blumberg RS
中科院分区：
文献类型：
--
作者：
Kaser A;Martínez-Naves E;Blumberg RS
概述细胞应激反应在炎症性肠病（IBD）中的新作用。未折叠蛋白反应（UPR）是一种原始的细胞通路，在响应内质网应激并调节自噬时参与。肠内的高分泌细胞，如Paneth细胞和杯状细胞，特别容易受到内质网应激的影响，并且非常依赖正常运作的UPR来维持细胞活力和体内平衡。UPR组成部分（如XBP1、ARG2、ORMDL3）、编码依赖于强大分泌途径的蛋白质的基因（如MUC2、HLAB27）和产生UPR紊乱的环境因素（如微生物产物和炎症细胞因子）中的原发性遗传异常是肠道炎症初级发展和/或持续存在的重要因素。内质网应激是IBD及其他肠道炎症性疾病相关肠道炎症发展的重要新途径。
To provide an overview of the emerging role of cellular stress responses in inflammatory bowel disease (IBD). The unfolded protein response (UPR) is a primitive cellular pathway that is engaged when responding to endoplasmic reticulum stress and regulates autophagy. Highly secretory cells such as Paneth cells and goblet cells in the intestines are particularly susceptible to endoplasmic reticulum stress and are exceedingly dependent upon a properly functioning UPR to maintain cellular viability and homeostasis. Primary genetic abnormalities within the components of the UPR (e.g. XBP1, ARG2, ORMDL3), genes that encode proteins reliant upon a robust secretory pathway (e.g. MUC2, HLAB27) and environmental factors that create disturbances in the UPR (e.g. microbial products and inflammatory cytokines) are important factors in the primary development and/or perpetuation of intestinal inflammation. Endoplasmic reticulum stress is an important new pathway involved in the development of intestinal inflammation associated with IBD and likely other intestinal inflammatory disorders.