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Antioxidants
Special Issues
Oxidative Stress and Redox Regulation in Chronic Inflammatory Disorders
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Oxidative Stress and Redox Regulation in Chronic Inflammatory Disorders

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: 31 May 2024 | Viewed by 812

Special Issue Editor

Dr. Emma Borrelli

E-Mail Website
Guest Editor
Department of Medical Biotechnologies, University of Siena, 53100 Siena, Italy
Interests: redox modulator; ozone therapy; oxidative stress in chronic diseases; antioxidants; anti-inflammatory agents; gaseous signaling molecules
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress and cellular redox regulation play a key role in the pathophysiological processes of a wide range of chronic diseases, such as cardiovascular diseases, chronic obstructive pulmonary disease and neurodegenerative diseases. It has been reported in a large number of clinical and experimental studies that reactive oxygen species (ROS) act at a low concentration as signalling molecules in several physiological cellular functions, for example in growth and inflammatory regulation, but an overproduction of ROS induces irreversible functional alterations or complete destruction in cells and organs.

For this reason, a better understanding of ROS-metabolising systems and redox regulation represents a chance to develop better therapeutic options for the treatment of chronic diseases that can replace, for example, a simple exogenous antioxidant administration that failed to restore the cellular functions and oxidative balance.

This Special Issue could be an opportunity for the scientific community to provide original research articles, clinical reports and review articles that cover a large range of fields, such as biochemistry, pathophysiology and oxidative stress and redox regulation therapy to treat chronic diseases.

Dr. Emma Borrelli
Guest Editor

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

  • redox regulation
  • reactive oxygen species
  • chronic diseases
  • cardiovascular diseases
  • obstructive pulmonary disease
  • neurodegenerative diseases

Published Papers (2 papers)

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Research

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17 pages, 3608 KiB  
Article
Redox Regulation of LAT Enhances T Cell-Mediated Inflammation
by Jaime James, Ana Coelho, Gonzalo Fernandez Lahore, Clara M. Hernandez, Florian Forster, Bernard Malissen and Rikard Holmdahl
Antioxidants 2024, 13(4), 499; https://doi.org/10.3390/antiox13040499 - 22 Apr 2024
Viewed by 299
Abstract
The positional cloning of single nucleotide polymorphisms (SNPs) of the neutrophil cytosolic factor 1 (Ncf1) gene, advocating that a low oxidative burst drives autoimmune disease, demands an understanding of the underlying molecular causes. A cellular target could be T cells, which [...] Read more.
The positional cloning of single nucleotide polymorphisms (SNPs) of the neutrophil cytosolic factor 1 (Ncf1) gene, advocating that a low oxidative burst drives autoimmune disease, demands an understanding of the underlying molecular causes. A cellular target could be T cells, which have been shown to be regulated by reactive oxygen species (ROS). However, the pathways by which ROS mediate T cell signaling remain unclear. The adaptor molecule linker for activation of T cells (LAT) is essential for coupling T cell receptor-mediated antigen recognition to downstream responses, and it contains several cysteine residues that have previously been suggested to be involved in redox regulation. To address the possibility that ROS regulate T cell-dependent inflammation through LAT, we established a mouse strain with cysteine-to-serine mutations at positions 120 and 172 (LATSS). We found that redox regulation of LAT through C120 and C172 mediate its localization and phosphorylation. LATSS mice had reduced numbers of double-positive thymocytes and naïve peripheral T cells. Importantly, redox insensitivity of LAT enhanced T cell-dependent autoimmune inflammation in collagen-induced arthritis (CIA), a mouse model of rheumatoid arthritis (RA). This effect was reversed on an NCF1-mutated (NCF1m1j), ROS-deficient, background. Overall, our data show that LAT is redox-regulated, acts to repress T cell activation, and is targeted by ROS induced by NCF1 in antigen-presenting cells (APCs). Full article
(This article belongs to the Special Issue Oxidative Stress and Redox Regulation in Chronic Inflammatory Disorders)
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Review

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30 pages, 2818 KiB  
Review
Elucidating the Molecular Pathways and Therapeutic Interventions of Gaseous Mediators in the Context of Fibrosis
by Aohan Li, Siyuan Wu, Qian Li, Qianqian Wang and Yingqing Chen
Antioxidants 2024, 13(5), 515; https://doi.org/10.3390/antiox13050515 - 25 Apr 2024
Viewed by 221
Abstract
Fibrosis, a pathological alteration of the repair response, involves continuous organ damage, scar formation, and eventual functional failure in various chronic inflammatory disorders. Unfortunately, clinical practice offers limited treatment strategies, leading to high mortality rates in chronic diseases. As part of investigations into [...] Read more.
Fibrosis, a pathological alteration of the repair response, involves continuous organ damage, scar formation, and eventual functional failure in various chronic inflammatory disorders. Unfortunately, clinical practice offers limited treatment strategies, leading to high mortality rates in chronic diseases. As part of investigations into gaseous mediators, or gasotransmitters, including nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S), numerous studies have confirmed their beneficial roles in attenuating fibrosis. Their therapeutic mechanisms, which involve inhibiting oxidative stress, inflammation, apoptosis, and proliferation, have been increasingly elucidated. Additionally, novel gasotransmitters like hydrogen (H2) and sulfur dioxide (SO2) have emerged as promising options for fibrosis treatment. In this review, we primarily demonstrate and summarize the protective and therapeutic effects of gaseous mediators in the process of fibrosis, with a focus on elucidating the underlying molecular mechanisms involved in combating fibrosis. Full article
(This article belongs to the Special Issue Oxidative Stress and Redox Regulation in Chronic Inflammatory Disorders)
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