1. ER Stress: A Therapeutic Target in Rheumatoid Arthritis?
- Author
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Rahmati M, Moosavi MA, and McDermott MF
- Subjects
- Animals, Arthritis, Rheumatoid metabolism, Endoplasmic Reticulum drug effects, Endoplasmic Reticulum metabolism, Humans, Antirheumatic Agents pharmacology, Arthritis, Rheumatoid drug therapy, Endoplasmic Reticulum Stress drug effects, Endoplasmic Reticulum-Associated Degradation drug effects
- Abstract
Diverse physiological and pathological conditions that impact on protein folding of the endoplasmic reticulum (ER) cause ER stress. The unfolded protein response (UPR) and the ER-associated degradation (ERAD) pathway are activated to cope with ER stress. In rheumatoid arthritis (RA), inflammation and ER stress work in parallel by driving inflammatory cells to release cytokines that induce chronic ER stress pathways. This chronic ER stress may contribute to the pathogenesis of RA through synoviocyte proliferation and proinflammatory cytokine production. Therefore, ER stress pathways and their constituent elements are attractive targets for RA drug development. In this review, we integrate current knowledge of the contribution of ER stress to the overall pathogenesis of RA, and suggest some therapeutic implications of these discoveries., (Copyright © 2018 Elsevier Ltd. All rights reserved.)
- Published
- 2018
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