Endoplasmic Reticulum Stress in Systemic Lupus Erythematosus and Lupus Nephritis: Potential Therapeutic Target
Systemic lupus erythematosus (SLE) is a complex autoimmune disease. Approximately one-third to two-thirds of the patients with SLE progress to lupus nephritis (LN). The pathogenesis of SLE and LN has not yet been fully elucidated, and effective treatment for both conditions is lacking. The endoplasm...
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Hindawi Limited
2023-01-01
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Series: | Journal of Immunology Research |
Online Access: | http://dx.doi.org/10.1155/2023/7625817 |
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author | Hui-Yuan Li Li-Feng Huang Xiao-Rong Huang Dan Wu Xiao-Cui Chen Ji-Xin Tang Ning An Hua-Feng Liu Chen Yang |
author_facet | Hui-Yuan Li Li-Feng Huang Xiao-Rong Huang Dan Wu Xiao-Cui Chen Ji-Xin Tang Ning An Hua-Feng Liu Chen Yang |
author_sort | Hui-Yuan Li |
collection | DOAJ |
description | Systemic lupus erythematosus (SLE) is a complex autoimmune disease. Approximately one-third to two-thirds of the patients with SLE progress to lupus nephritis (LN). The pathogenesis of SLE and LN has not yet been fully elucidated, and effective treatment for both conditions is lacking. The endoplasmic reticulum (ER) is the largest intracellular organelle and is a site of protein synthesis, lipid metabolism, and calcium storage. Under stress, the function of ER is disrupted, and the accumulation of unfolded or misfolded proteins occurs in ER, resulting in an ER stress (ERS) response. ERS is involved in the dysfunction of B cells, macrophages, T cells, dendritic cells, neutrophils, and other immune cells, causing immune system disorders, such as SLE. In addition, ERS is also involved in renal resident cell injury and contributes to the progression of LN. The molecular chaperones, autophagy, and proteasome degradation pathways inhibit ERS and restore ER homeostasis to improve the dysfunction of immune cells and renal resident cell injury. This may be a therapeutic strategy for SLE and LN. In this review, we summarize advances in this field. |
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language | English |
last_indexed | 2024-03-12T01:57:03Z |
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spelling | doaj.art-43d107ac5eb94339bc2096cc07c27d232023-09-08T00:00:04ZengHindawi LimitedJournal of Immunology Research2314-71562023-01-01202310.1155/2023/7625817Endoplasmic Reticulum Stress in Systemic Lupus Erythematosus and Lupus Nephritis: Potential Therapeutic TargetHui-Yuan Li0Li-Feng Huang1Xiao-Rong Huang2Dan Wu3Xiao-Cui Chen4Ji-Xin Tang5Ning An6Hua-Feng Liu7Chen Yang8Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable DiseasesGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable DiseasesGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable DiseasesGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable DiseasesGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable DiseasesGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable DiseasesGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable DiseasesGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable DiseasesGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable DiseasesSystemic lupus erythematosus (SLE) is a complex autoimmune disease. Approximately one-third to two-thirds of the patients with SLE progress to lupus nephritis (LN). The pathogenesis of SLE and LN has not yet been fully elucidated, and effective treatment for both conditions is lacking. The endoplasmic reticulum (ER) is the largest intracellular organelle and is a site of protein synthesis, lipid metabolism, and calcium storage. Under stress, the function of ER is disrupted, and the accumulation of unfolded or misfolded proteins occurs in ER, resulting in an ER stress (ERS) response. ERS is involved in the dysfunction of B cells, macrophages, T cells, dendritic cells, neutrophils, and other immune cells, causing immune system disorders, such as SLE. In addition, ERS is also involved in renal resident cell injury and contributes to the progression of LN. The molecular chaperones, autophagy, and proteasome degradation pathways inhibit ERS and restore ER homeostasis to improve the dysfunction of immune cells and renal resident cell injury. This may be a therapeutic strategy for SLE and LN. In this review, we summarize advances in this field.http://dx.doi.org/10.1155/2023/7625817 |
spellingShingle | Hui-Yuan Li Li-Feng Huang Xiao-Rong Huang Dan Wu Xiao-Cui Chen Ji-Xin Tang Ning An Hua-Feng Liu Chen Yang Endoplasmic Reticulum Stress in Systemic Lupus Erythematosus and Lupus Nephritis: Potential Therapeutic Target Journal of Immunology Research |
title | Endoplasmic Reticulum Stress in Systemic Lupus Erythematosus and Lupus Nephritis: Potential Therapeutic Target |
title_full | Endoplasmic Reticulum Stress in Systemic Lupus Erythematosus and Lupus Nephritis: Potential Therapeutic Target |
title_fullStr | Endoplasmic Reticulum Stress in Systemic Lupus Erythematosus and Lupus Nephritis: Potential Therapeutic Target |
title_full_unstemmed | Endoplasmic Reticulum Stress in Systemic Lupus Erythematosus and Lupus Nephritis: Potential Therapeutic Target |
title_short | Endoplasmic Reticulum Stress in Systemic Lupus Erythematosus and Lupus Nephritis: Potential Therapeutic Target |
title_sort | endoplasmic reticulum stress in systemic lupus erythematosus and lupus nephritis potential therapeutic target |
url | http://dx.doi.org/10.1155/2023/7625817 |
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