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Endoplasmic reticulum stress: implications for inflammatory bowel disease pathogenesis.

机译:内质网应激:对炎症性肠病发病机制的影响。

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PURPOSE OF REVIEW: To provide an overview of the emerging role of cellular stress responses in inflammatory bowel disease (IBD). RECENT FINDINGS: 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. SUMMARY: Endoplasmic reticulum stress is an important new pathway involved in the development of intestinal inflammation associated with IBD and likely other intestinal inflammatory disorders.
机译:审查目的:概述炎症应激性肠病(IBD)中细胞应激反应的新兴作用。最近的发现:未折叠的蛋白质反应(UPR)是一种原始细胞途径,在响应内质网应激并调节自噬时参与其中。肠道中高度分泌的细胞(例如Paneth细胞和杯状细胞)特别容易受到内质网应激的影响,并且过度依赖正常运转的UPR来维持细胞活力和体内平衡。 UPR组件内的主要遗传异常(例如XBP1,ARG2,ORMDL3),编码依赖于强大的分泌途径的蛋白质的基因(例如MUC2,HLAB27)和造成UPR紊乱的环境因素(例如微生物产物和炎性细胞因子) )是肠道炎症的主要发展和/或永存的重要因素。摘要:内质网应激是与IBD相关的肠道炎症和其他可能的肠道炎症疾病发展的重要新途径。

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