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Er Stress: A Therapeutic Target in Rheumatoid Arthritis? Publisher Pubmed



Rahmati M1 ; Moosavi MA2 ; Mcdermott MF3
Authors
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Authors Affiliations
  1. 1. Cancer Biology Research Center, Cancer Institute of Iran, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Molecular Medicine, Institute of Medical Biotechnology, National Institute of Genetic Engineering and Biotechnology, P.O Box:14965/161, Tehran, Iran
  3. 3. Leeds Institute of Rheumatic and Musculoskeletal Medicine (LIRMM), Wellcome Trust Brenner Building, St James's University Hospital, Beckett Street, Leeds, LS9 7TF, United Kingdom

Source: Trends in Pharmacological Sciences Published:2018


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. © 2018 Elsevier Ltd
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