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12.4
6.6
Journals
Antioxidants
Special Issues
Oxidative Stress and Airway Diseases
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Oxidative Stress and Airway Diseases

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 July 2026 | Viewed by 1398

Special Issue Editor

Dr. Miguel Santibáñez-Margüello

E-Mail Website
Guest Editor
1. Instituto de Investigación Marqués de Valdecilla (IDIVAL), University of Cantabria, Santander, Spain
2. CIBER of Respiratory Diseases (CIBERES), Instituto de Salud Carlos III, Madrid, Spain
Interests: respiratory system; public; environmental and occupational health

Special Issue Information

Dear Colleagues,

Oxidative stress refers to an imbalance between reactive oxygen species (ROS) and the endogenous antioxidant capacity, which can lead to the oxidation of lipids and proteins, as well as damage to DNA and RNA. This contributes to enhanced airway and systemic inflammatory responses and plays a key role in the development and clinical course of airway diseases.

This disruption in redox homeostasis may arise as a consequence of environmental airborne exposure to particulate matter (PM) with high oxidative potential; from impaired endogenous antioxidant mechanisms; or as a result of the intrinsic pathophysiological processes of the airway disease itself. As an example, chronic inflammation in asthma is mediated by the activation of granulocytes, with an invasion of the bronchial mucosa. In addition to the ROS incorporated by the airborne PM, activated macrophages, neutrophils, and eosinophils are able to release ROS. Therefore, it is not clear whether, in terms of ROS, the contribution of PM inhalation is greater than that of the inflammatory cells themselves.

This Special Issue welcomes the submission of original research articles, reviews, meta-analyses, and clinical trial results exploring any aspect of oxidative stress in the physiopathogenesis of airway diseases, as well as antioxidant-based therapeutic interventions.

We look forward to your contributions.

Dr. Miguel Santibáñez-Margüello
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 250 words) can be sent to the Editorial Office for assessment.

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

  • oxidative stress
  • asthma
  • chronic obstructive pulmonary disease (COPD)
  • particulate matter oxidative potential (PM-OP)

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Published Papers (2 papers)

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Research

23 pages, 14922 KB  
Article
Pneumocystis Colonization Is Associated with Enhanced Pulmonary Remodeling and Activation of Redox-Responsive Pathways in a COPD Experimental Model
by Andrea Méndez, Krishna Coronado and Diego A. Rojas
Antioxidants 2026, 15(5), 526; https://doi.org/10.3390/antiox15050526 - 22 Apr 2026
Viewed by 361
Abstract
Chronic Obstructive Pulmonary Disease (COPD) is characterized by persistent inflammation and structural alterations in the lung triggered mainly by oxidative stress. Colonization by the opportunistic fungus Pneumocystis has been associated with worse clinical outcomes in COPD, yet its role in airway remodeling remains [...] Read more.
Chronic Obstructive Pulmonary Disease (COPD) is characterized by persistent inflammation and structural alterations in the lung triggered mainly by oxidative stress. Colonization by the opportunistic fungus Pneumocystis has been associated with worse clinical outcomes in COPD, yet its role in airway remodeling remains unclear. To this end, an elastase-induced COPD model was established, followed by colonization with Pneumocystis. Lung tissue was analyzed histologically and molecularly to assess epithelial thickness, alveolar morphometric parameters (mean linear intercept [MLI], D0, D1, D2), inflammation, collagen deposition, and the expression of remodeling and oxidative stress markers. Emphysematous damage parameters MLI, D0, D1, and D2 were markedly elevated in co-exposed animals, indicating enhanced alveolar enlargement. Animals with COPD and Pneumocystis colonization showed a significant increase in airway inflammation compared with control, COPD, and Pneumocystis groups. Airway epithelial thickness, mucus metaplasia, and collagen deposition exhibited a summative increase in the COPD/Pneumocystis group. Redox-responsive markers, such as superoxide dismutase (SOD) and catalase, were upregulated. Moreover, protein and mRNA levels of nuclear factor erythroid 2–related factor 2 (Nrf2) and its downstream gene heme oxygenase-1 (Hmox1) were significantly increased, with the strongest activation observed in co-exposed animals. Integrative correlation analysis showed that Pneumocystis burden positively correlated with lung damage, inflammation, and epithelial remodeling. These structural alterations were accompanied by coordinated activation of the antioxidant pathway Nrf2. Taken together, Pneumocystis colonization is associated with enhanced pulmonary remodeling and modulation of antioxidant signaling in experimental COPD, promoting structural and molecular changes that may contribute to disease progression. These findings suggest that Pneumocystis acts as an amplifying factor in COPD-associated lung damage. Full article
(This article belongs to the Special Issue Oxidative Stress and Airway Diseases)
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18 pages, 2158 KB  
Article
Sputum Glutaredoxin 1 and Protein S-Glutathionylation in COPD
by Ine Kuipers, Renske Krijgsman, Renaud Louis, Jean-Louis Corhay, Thibault Azevedo Mendes, Guy G. Brusselle, Ken R. Bracke and Niki L. Reynaert
Antioxidants 2026, 15(3), 330; https://doi.org/10.3390/antiox15030330 - 6 Mar 2026
Viewed by 637
Abstract
Alterations in glutathione and its metabolism contribute to oxidative stress in COPD, but the role of S-glutathionylation (PSSG) and its major regulator glutaredoxin 1 (Grx1) remains unclear. This study investigated the Grx1/PSSG axis in sputum of COPD patients and its associations with lung [...] Read more.
Alterations in glutathione and its metabolism contribute to oxidative stress in COPD, but the role of S-glutathionylation (PSSG) and its major regulator glutaredoxin 1 (Grx1) remains unclear. This study investigated the Grx1/PSSG axis in sputum of COPD patients and its associations with lung function and inflammation, as well as Grx1 secretion in mouse models and in cell culture. In patients with an acute exacerbation, PSSG levels were significantly decreased in sputum, while Grx1 protein and total Grx activity were increased compared to stable COPD. No differences were observed between healthy smokers and stable patients. PSSG levels correlated negatively with sputum neutrophils, IL-8 and IL-1β, but positively with lung function parameters, whereas Grx1 showed the opposite pattern. Enhanced Grx1 levels were also detected in bronchoalveolar lavage fluid from mice exposed to cigarette smoke or chronic pulmonary inflammation. Moreover, epithelial cells and macrophages secreted Grx1 in response to pro-inflammatory mediators, and Grx1 modulated expression of MMPs by macrophages in vitro and in vivo. In conclusion, this study identifies the Grx1/PSSG redox axis as a potential important factor in COPD pathogenesis, especially during exacerbations. Further research should examine in more detail the intricate relation of extracellular Grx1 with lung function and inflammation. Full article
(This article belongs to the Special Issue Oxidative Stress and Airway Diseases)
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