Journal
TRENDS IN MOLECULAR MEDICINE
Volume 18, Issue 10, Pages 589-598Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2012.06.010
Keywords
ER stress; cancer; inflammation; obesity; diabetes; inflammatory bowel disease; immunity; therapeutics; airway disease
Funding
- GOA [GOA/11/2010-2015]
- Interuniversity Attraction Poles Programme [IAP6/18]
- Belgian State, Science Policy Office
- Fund for Scientific Research Flanders [FWO-Vlaanderen] [G072810N, 3G067512, 31507110]
- FWO-Vlaanderen Research in the Vandenabeele unit
- Flanders Institute for Biotechnology (VIB)
- European grants [MRTN-CT-035624, FP7-200767]
- Flemish grants (Fonds Wetenschappelijke Onderzoek Vlaanderen) [3G.0218.06]
- Ghent University
- Flemish Government [BOF09/01M00709]
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Different lines of research have revealed that pathways activated by the endoplasmic reticulum (ER) stress response induce sterile inflammation. When activated, all three sensors of the unfolded protein response (UPR), PERK, IRE1, and ATF6, participate in upregulating inflammatory processes. ER stress in various cells plays an important role in the pathogenesis of several diseases, including obesity, type 2 diabetes, cancer, and intestinal bowel and airway diseases. Moreover, it has been suggested that ER stress-induced inflammation contributes substantially to disease progression. However, this generalization can be challenged at least in the case of cancer. In this review, we emphasize that ER stress can either aid or impede disease progression via inflammatory pathways depending on the cell type, disease stage, and type of ER stressor.
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