Department of Medicine II (Gastroenterology & Hepatology), Innsbruck Medical University, Innsbruck, Austria.
Curr Opin Gastroenterol. 2010 Jul;26(4):318-26. doi: 10.1097/MOG.0b013e32833a9ff1.
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.
阐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，在应对内质网应激时被激活，调节自噬。肠道中高度分泌的细胞，如潘氏细胞和杯状细胞，特别容易受到内质网应激的影响，并且极其依赖于功能正常的 UPR 来维持细胞活力和内稳态。UPR 成分（如 XBP1、ARG2、ORMDL3）内的主要遗传异常、编码依赖强大分泌途径的蛋白质的基因（如 MUC2、HLA-B27）以及在内质网应激中产生干扰的环境因素（如微生物产物和炎症细胞因子）是 IBD 相关肠道炎症的主要发展和/或持续的重要因素。
内质网应激是与 IBD 相关的肠道炎症发展中的一个重要新途径，可能与其他肠道炎症性疾病有关。
