Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases

被引:32
|
作者
Scavuzzi, Bruna Miglioranza [1 ]
Holoshitz, Joseph [1 ]
机构
[1] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA
关键词
rheumatic diseases; endoplasmic reticulum stress; ER stress inhibit; oxidative stress; antioxidants; SYSTEMIC-LUPUS-ERYTHEMATOSUS; ER CHAPERONE GRP78/BIP; REGULATORY T-CELLS; TRANSCRIPTION FACTOR; B-CELL; 4-PHENYLBUTYRIC ACID; PROTEIN BIP; MITOCHONDRIAL HYPERPOLARIZATION; MOLECULAR CHAPERONES; PATHOGENIC ROLE;
D O I
10.3390/antiox11071306
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: The endoplasmic reticulum (ER) is a multi-functional organelle responsible for cellular homeostasis, protein synthesis, folding and secretion. It has been increasingly recognized that the loss of ER homeostasis plays a central role in the development of autoimmune inflammatory disorders, such as rheumatic diseases. Purpose/Main contents: Here, we review current knowledge of the contribution of ER stress to the pathogenesis of rheumatic diseases, with a focus on rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). We also review the interplay between protein folding and formation of reactive oxygen species (ROS), where ER stress induces oxidative stress (OS), which further aggravates the accumulation of misfolded proteins and oxidation, in a vicious cycle. Intervention studies targeting ER stress and oxidative stress in the context of rheumatic diseases are also reviewed. Conclusions: Loss of ER homeostasis is a significant factor in the pathogeneses of RA and SLE. Targeting ER stress, unfolded protein response (UPR) pathways and oxidative stress in these diseases both in vitro and in animal models have shown promising results and deserve further investigation.
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收藏
页数:19
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