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Antioxidants
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The Role of Oxidative Stress in Chronic Diseases: Focus on...
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The Role of Oxidative Stress in Chronic Diseases: Focus on Lupus and Rheumatoid Arthritis

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (15 April 2022) | Viewed by 21841

Special Issue Editors

Dr. Isaias Dichi

E-Mail Website
Guest Editor
Department of Internal Medicine, University of Londrina, Londrina, Paraná, Brazil
Interests: oxidative stress; inflammation; immunoinflammatory disorders; metabolic disorders; nutritional intervention
Special Issues, Collections and Topics in MDPI journals
Dr. Bruna Miglioranza Scavuzzi

E-Mail Website
Guest Editor
Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA
Interests: oxidative stress; antioxidants; inflammation; autoimmune disorders; mitochondria
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

 Reactive oxygen species (ROS) are products of cellular metabolism that, in controlled quantities, modulate several physiological aspects of cell function and are required for signaling pathways. Nonetheless, when excessive ROS production occurs, or when their elimination by antioxidant mechanisms is impaired, they may accumulate and become pathogenic, a condition known as oxidative stress. Oxidative stress plays an important role in the development and exacerbation of several inflammatory, chronic and autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus (lupus). Recent advances in the understanding of the pathological action of oxidative species, as well as promising findings involving prevention and even treatment of rheumatic diseases with antioxidant therapies, have highlighted the potential of redox homeostasis for the maintenance of physiological functions and the prevention of numerous redox-dependent pathologies.

The aim of this Special Issue is to provide Antioxidants’ readers with updated research considering oxidative stress in the development and exacerbation of chronic rheumatic diseases, with a focus mainly on lupus and rheumatoid arthritis. In vitro studies investigating molecular mechanisms, as well as in vivo studies considering oxidative stress biomarkers, and the effect of antioxidant treatments in rheumatic diseases will be considered for this issue.

Dr. Isaias Dichi
Dr. Bruna Miglioranza Scavuzzi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • lupus
  • rheumatoid arthritis
  • oxidative stress
  • inflammation
  • antioxidants

Published Papers (6 papers)

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Research

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20 pages, 3453 KiB  
Article
Sp1 S-Sulfhydration Induced by Hydrogen Sulfide Inhibits Inflammation via HDAC6/MyD88/NF-κB Signaling Pathway in Adjuvant-Induced Arthritis
by Meng Li, Wei Hu, Ran Wang, Zhaoyi Li, Yue Yu, Yue Zhuo, Yida Zhang, Zhou Wang, Yuanye Qiu, Keyuan Chen, Qian Ding, Wei Qi, Menglin Zhu and Yizhun Zhu
Antioxidants 2022, 11(4), 732; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11040732 - 07 Apr 2022
Cited by 13 | Viewed by 2555
Abstract
Histone deacetylase 6 (HDAC6) acts as a regulator of the nuclear factor kappa-B (NF-κB) signaling pathway by deacetylating the non-histone protein myeloid differentiation primary response 88 (MyD88) at lysine residues, which is an adapter protein for the Toll-like receptor (TLR) and interleukin (IL)-1β [...] Read more.
Histone deacetylase 6 (HDAC6) acts as a regulator of the nuclear factor kappa-B (NF-κB) signaling pathway by deacetylating the non-histone protein myeloid differentiation primary response 88 (MyD88) at lysine residues, which is an adapter protein for the Toll-like receptor (TLR) and interleukin (IL)-1β receptor. Over-activated immune responses, induced by infiltrated immune cells, excessively trigger the NF-κB signaling pathway in other effector cells and contribute to the development of rheumatoid arthritis (RA). It has also been reported that HDAC6 can promote the activation of the NF-κB signaling pathway. In the present study, we showed that HDAC6 protein level was increased in the synovium tissues of adjuvant-induced arthritis rats. In addition, hydrogen sulfide (H2S) donor S-propargyl-cysteine (SPRC) can inhibit HDAC6 expression and alleviate inflammatory response in vivo. In vitro study revealed that HDAC6 overexpression activated the NF-κB signaling pathway by deacetylating MyD88. Meanwhile, sodium hydrosulfide (NaHS) or HDAC6 inhibitor tubastatin A (tubA) suppressed the pro-inflammatory function of HDAC6. Furthermore, the reduced expression of HDAC6 appeared to result from transcriptional inhibition by S-sulfhydrating specificity protein 1 (Sp1), which is a transcription factor of HDAC6. Our results demonstrate that Sp1 can regulate HDAC6 expression, and S-sulfhydration of Sp1 by antioxidant molecular H2S ameliorates RA progression via the HDAC6/MyD88/NF-κB signaling pathway. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Chronic Diseases: Focus on Lupus and Rheumatoid Arthritis)
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18 pages, 63789 KiB  
Article
Glycan Activation of Clec4b Induces Reactive Oxygen Species Protecting against Neutrophilia and Arthritis
by Mike Aoun, Xiaojie Cai, Bingze Xu, Gonzalo Fernandez Lahore, Michael Yi Bonner, Yibo He, Liselotte Bäckdahl and Rikard Holmdahl
Antioxidants 2022, 11(1), 12; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11010012 - 22 Dec 2021
Cited by 1 | Viewed by 2250
Abstract
Animal models for complex diseases are needed to position and analyze the function of interacting genes. Previous positional cloning identified Ncf1 and Clec4b to be major regulators of arthritis models in rats. Here, we investigate epistasis between Ncf1 and Clec4b, two major regulators [...] Read more.
Animal models for complex diseases are needed to position and analyze the function of interacting genes. Previous positional cloning identified Ncf1 and Clec4b to be major regulators of arthritis models in rats. Here, we investigate epistasis between Ncf1 and Clec4b, two major regulators of arthritis in rats. We find that Clec4b and Ncf1 exert an additive effect on arthritis given by their joint ability to regulate neutrophils. Both genes are highly expressed in neutrophils, together regulating neutrophil availability and their capacity to generate reactive oxygen species. Using a glycan array, we identify key ligands of Clec4b and demonstrate that Clec4b-specific stimulation triggers neutrophils into oxidative burst. Our observations highlight Clec4b as an important regulator of neutrophils and demonstrate how epistatic interactions affect the susceptibility to, and severity of, autoimmune arthritis. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Chronic Diseases: Focus on Lupus and Rheumatoid Arthritis)
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23 pages, 2554 KiB  
Article
Gut Microbiota Has a Crucial Role in the Development of Hypertension and Vascular Dysfunction in Toll-like Receptor 7-Driven Lupus Autoimmunity
by Néstor de la Visitación, Iñaki Robles-Vera, Javier Moleón, Cristina González-Correa, Nazaret Aguilera-Sánchez, Marta Toral, Manuel Gómez-Guzmán, Manuel Sánchez, Rosario Jiménez, Natividad Martin-Morales, Francisco O’Valle, Miguel Romero and Juan Duarte
Antioxidants 2021, 10(9), 1426; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10091426 - 07 Sep 2021
Cited by 8 | Viewed by 3486
Abstract
Our group has investigated the involvement of gut microbiota in hypertension in a murine model of systemic lupus erythematosus induced by Toll-like receptor (TLR)-7 activation. Female BALB/c mice were randomly assigned to four experimental groups: an untreated control (CTR), a group treated with [...] Read more.
Our group has investigated the involvement of gut microbiota in hypertension in a murine model of systemic lupus erythematosus induced by Toll-like receptor (TLR)-7 activation. Female BALB/c mice were randomly assigned to four experimental groups: an untreated control (CTR), a group treated with the TLR7 agonist imiquimod (IMQ), IMQ-treated with vancomycin, and IMQ-treated with a cocktail of broad-spectrum antibiotics. We carried out faecal microbiota transplant (FMT) from donor CTR or IMQ mice to recipient IMQ or CTR animals, respectively. Vancomycin inhibited the increase in blood pressure; improved kidney injury, endothelial function, and oxidative stress; and reduced T helper (Th)17 infiltration in aortas from IMQ-treated mice. The rise in blood pressure and vascular complications present in IMQ mice were also observed in the CTR mice recipients of IMQ microbiota. Reduced relative populations of Sutterella and Anaerovibrio were associated with high blood pressure in our animals, which were increased after stool transplantation of healthy microbiota to IMQ mice. The reduced endothelium-dependent vasodilator responses to acetylcholine induced by IMQ microbiota were normalized after interleukin-17 neutralization. In conclusion, gut microbiota plays a role in the TLR7-driven increase in Th17 cell, endothelial dysfunction, vascular inflammation, and hypertension. The vascular changes induced by IMQ microbiota were initiated by Th17 infiltrating the vasculature. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Chronic Diseases: Focus on Lupus and Rheumatoid Arthritis)
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Review

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19 pages, 1105 KiB  
Review
Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases
by Bruna Miglioranza Scavuzzi and Joseph Holoshitz
Antioxidants 2022, 11(7), 1306; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11071306 - 29 Jun 2022
Cited by 19 | Viewed by 3128
Abstract
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Chronic Diseases: Focus on Lupus and Rheumatoid Arthritis)
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27 pages, 2018 KiB  
Review
The Role of Reactive Oxygen Species in the Rheumatoid Arthritis-Associated Synovial Microenvironment
by Xing Wang, Danping Fan, Xiaoxue Cao, Qinbin Ye, Qiong Wang, Mengxiao Zhang and Cheng Xiao
Antioxidants 2022, 11(6), 1153; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11061153 - 13 Jun 2022
Cited by 31 | Viewed by 5436
Abstract
Rheumatoid arthritis (RA) is an inflammatory disease that begins with a loss of tolerance to modified self-antigens and immune system abnormalities, eventually leading to synovitis and bone and cartilage degradation. Reactive oxygen species (ROS) are commonly used as destructive or modifying agents of [...] Read more.
Rheumatoid arthritis (RA) is an inflammatory disease that begins with a loss of tolerance to modified self-antigens and immune system abnormalities, eventually leading to synovitis and bone and cartilage degradation. Reactive oxygen species (ROS) are commonly used as destructive or modifying agents of cellular components or they act as signaling molecules in the immune system. During the development of RA, a hypoxic and inflammatory situation in the synovium maintains ROS generation, which can be sustained by increased DNA damage and malfunctioning mitochondria in a feedback loop. Oxidative stress caused by abundant ROS production has also been shown to be associated with synovitis in RA. The goal of this review is to examine the functions of ROS and related molecular mechanisms in diverse cells in the synovial microenvironment of RA. The strategies relying on regulating ROS to treat RA are also reviewed. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Chronic Diseases: Focus on Lupus and Rheumatoid Arthritis)
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30 pages, 1156 KiB  
Review
Mitochondrial Dysfunction and Oxidative Stress in Rheumatoid Arthritis
by María José López-Armada, Jennifer Adriana Fernández-Rodríguez and Francisco Javier Blanco
Antioxidants 2022, 11(6), 1151; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11061151 - 12 Jun 2022
Cited by 26 | Viewed by 3988
Abstract
Control of excessive mitochondrial oxidative stress could provide new targets for both preventive and therapeutic interventions in the treatment of chronic inflammation or any pathology that develops under an inflammatory scenario, such as rheumatoid arthritis (RA). Increasing evidence has demonstrated the role of [...] Read more.
Control of excessive mitochondrial oxidative stress could provide new targets for both preventive and therapeutic interventions in the treatment of chronic inflammation or any pathology that develops under an inflammatory scenario, such as rheumatoid arthritis (RA). Increasing evidence has demonstrated the role of mitochondrial alterations in autoimmune diseases mainly due to the interplay between metabolism and innate immunity, but also in the modulation of inflammatory response of resident cells, such as synoviocytes. Thus, mitochondrial dysfunction derived from several danger signals could activate tricarboxylic acid (TCA) disruption, thereby favoring a vicious cycle of oxidative/mitochondrial stress. Mitochondrial dysfunction can act through modulating innate immunity via redox-sensitive inflammatory pathways or direct activation of the inflammasome. Besides, mitochondria also have a central role in regulating cell death, which is deeply altered in RA. Additionally, multiple evidence suggests that pathological processes in RA can be shaped by epigenetic mechanisms and that in turn, mitochondria are involved in epigenetic regulation. Finally, we will discuss about the involvement of some dietary components in the onset and progression of RA. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Chronic Diseases: Focus on Lupus and Rheumatoid Arthritis)
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