School of Applied Sciences, Edinburgh Napier University, Edinburgh, United Kingdom.
Child Life and Health, University of Edinburgh, Edinburgh, United Kingdom.
Inflamm Bowel Dis. 2019 Mar 14;25(4):661-671. doi: 10.1093/ibd/izy380.
Inflammatory bowel disease (IBD), which includes Crohn's disease (CD) and ulcerative colitis, is characterized by chronic inflammation of the gastrointestinal tract. The etiology involves a combination of genetic and environmental factors resulting in abnormal immune responses to intestinal microbiota. Genetic studies have strongly linked genes involved in autophagy to CD, and genes involved in the unfolded protein response (UPR) to IBD. The UPR is triggered in response to accumulation of misfolded proteins in the endoplasmic reticulum (ER), and autophagy plays a key role in relieving ER stress and restoring homeostasis. This review summarizes the known interactions between autophagy and the UPR and discusses the impact of these converging pathways on IBD pathogenesis. With a paucity of effective long-term treatments for IBD, targeting of synergistic pathways may provide novel and more effective therapeutic options.
炎症性肠病（IBD）包括克罗恩病（CD）和溃疡性结肠炎，其特征为胃肠道的慢性炎症。其病因涉及遗传和环境因素的共同作用，导致对肠道微生物群的异常免疫反应。遗传研究强烈提示自噬相关基因与 CD 相关， unfolded protein response（UPR）相关基因与 IBD 相关。UPR 是对内质网（ER）中错误折叠蛋白积累的反应，自噬在缓解 ER 应激和恢复内稳态方面发挥关键作用。本综述总结了自噬与 UPR 之间已知的相互作用，并讨论了这些趋同途径对 IBD 发病机制的影响。由于 IBD 缺乏有效的长期治疗方法，靶向协同途径可能提供新的、更有效的治疗选择。
