Institute of Clinical Molecular Biology, Christian-Albrechts-University Kiel, Rosalind-Franklin-Str. 12, 24105 Kiel, Germany.
Institute of Clinical Molecular Biology, Christian-Albrechts-University Kiel, Rosalind-Franklin-Str. 12, 24105 Kiel, Germany.
Biochim Biophys Acta Mol Cell Res. 2017 Nov;1864(11 Pt B):2183-2190. doi: 10.1016/j.bbamcr.2017.07.008. Epub 2017 Jul 21.
Endoplasmic reticulum (ER) stress and autophagy are tightly controlled cellular processes, which are responsible for maintaining protein homeostasis in a cell. Impairment of the interlinking pathways have been implicated in a number of human diseases, prominently in inflammatory bowel disease, where genetic variants in several independent autophagy and ER stress related loci have been associated to increased disease risk. Autophagy is a selective quality control process, which governs the integrity of the cell by removal of aged organelles and proteins via the lysosome, but recently has been shown to actively license the outcome of other signaling pathways by guiding the proteolytic removal of signaling protein complexes (adaptophagy). In this review, we summarize our knowledge on regulated proteolytic events involved in ER stress responses and autophagy, their interplay and potential regulatory effects with a particular focus on intestinal inflammation. This article is part of a Special Issue entitled: Proteolysis as a Regulatory Event in Pathophysiology edited by Stefan Rose-John.
内质网（ER）应激和自噬是紧密控制的细胞过程，负责维持细胞内的蛋白质平衡。连接途径的损伤与许多人类疾病有关，特别是在炎症性肠病中，几个独立的自噬和 ER 应激相关基因座的遗传变异与疾病风险增加有关。自噬是一种选择性的质量控制过程，通过溶酶体清除衰老的细胞器和蛋白质来维持细胞的完整性，但最近的研究表明，它通过指导信号蛋白复合物的蛋白水解去除（适应自噬），积极控制其他信号通路的结果。在这篇综述中，我们总结了我们对内质网应激反应和自噬中涉及的调节蛋白水解事件的了解，它们的相互作用以及与肠道炎症特别相关的潜在调节作用。本文是由 Stefan Rose-John 编辑的特刊“病理生理学中的蛋白水解作为调节事件”的一部分。
