Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1864, Issue 11, Pages 2183-2190Publisher
ELSEVIER
DOI: 10.1016/j.bbamcr.2017.07.008
Keywords
Autophagy; Inflammatory bowel disease; Er stress; Cell death; Proteolysis; Proteasome; Necroptosis
Categories
Funding
- Deutsche Forschungsgemeinschaft (DFG) [SFB877 B9]
- Cluster of Excellence Inflammation at Interfaces [ExC 306]
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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.
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