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Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases
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,...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9312221/ https://www.ncbi.nlm.nih.gov/pubmed/35883795 http://dx.doi.org/10.3390/antiox11071306 |
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author | Miglioranza Scavuzzi, Bruna Holoshitz, Joseph |
author_facet | Miglioranza Scavuzzi, Bruna Holoshitz, Joseph |
author_sort | Miglioranza Scavuzzi, Bruna |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9312221 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-93122212022-07-26 Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases Miglioranza Scavuzzi, Bruna Holoshitz, Joseph Antioxidants (Basel) Review 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. MDPI 2022-06-29 /pmc/articles/PMC9312221/ /pubmed/35883795 http://dx.doi.org/10.3390/antiox11071306 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Miglioranza Scavuzzi, Bruna Holoshitz, Joseph Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases |
title | Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases |
title_full | Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases |
title_fullStr | Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases |
title_full_unstemmed | Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases |
title_short | Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases |
title_sort | endoplasmic reticulum stress, oxidative stress, and rheumatic diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9312221/ https://www.ncbi.nlm.nih.gov/pubmed/35883795 http://dx.doi.org/10.3390/antiox11071306 |
work_keys_str_mv | AT miglioranzascavuzzibruna endoplasmicreticulumstressoxidativestressandrheumaticdiseases AT holoshitzjoseph endoplasmicreticulumstressoxidativestressandrheumaticdiseases |