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Antioxidants
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Redox Regulation in Pulmonary Diseases
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Redox Regulation in Pulmonary 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: closed (20 September 2022) | Viewed by 17092

Special Issue Editor

Dr. Agnes W. Boots

E-Mail Website
Guest Editor
Department of Pharmacology and Toxicology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands
Interests: redox signaling; chronic pulmonary diseases; fibrosis; epithelial damage and repair; redox modulation; dietary antioxidants; breath analysis

Special Issue Information

Dear Colleagues,

Contributions to this Special Issue may cover all aspects related to research on redox regulation in pulmonary fibrosis, including (but not limited to) cell-based assays; 3D in vitro models and organoids with, for example, epithelial cells, fibroblasts, or MSCs; lung on a chip; and in vivo animal or human studies exploring i) normal as well as dysfunctional pulmonary physiology, ii) irreversible pulmonary damage, and iii) impaired lung repair to further understand redox regulation in fibrosing lung diseases of known and unknown causes; in vitro and in vivo studies to examine the therapeutic potential of individual endogenous or exogenous antioxidants for fibrosing lung diseases of known and unknown causes; in vitro application of silencing and knockout techniques, biochemical assays, and redox assays to elaborate on pulmonary redox regulation in relation to lung damage, repair, and fibrosis.

Dr. Agnes W. Boots
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 signaling
  • Reactive oxygen species
  • Antioxidants
  • Cellular mechanisms
  • Pulmonary fibrosis
  • Chronic lung diseases
  • 3D in vitro models

Published Papers (7 papers)

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Research

Jump to: Review

14 pages, 3061 KiB  
Article
Differences in Treatment Response in Bronchial Epithelial Cells from Idiopathic Pulmonary Fibrosis (IPF) Patients: A First Step towards Personalized Medicine?
by C. Veith, M. A. Schneider, L. Maas, A. van der Vliet, F. J. van Schooten, M. Kreuter, M. Meister, A. W. Boots and N. Kahn
Antioxidants 2023, 12(2), 443; https://doi.org/10.3390/antiox12020443 - 10 Feb 2023
Viewed by 1580
Abstract
Idiopathic pulmonary fibrosis (IPF) has a detrimental prognosis despite antifibrotic therapies to which individual responses vary. IPF pathology is associated with oxidative stress, inflammation and increased activation of SRC family kinases (SFK). This pilot study evaluates individual responses to pirfenidone, nintedanib and SFK [...] Read more.
Idiopathic pulmonary fibrosis (IPF) has a detrimental prognosis despite antifibrotic therapies to which individual responses vary. IPF pathology is associated with oxidative stress, inflammation and increased activation of SRC family kinases (SFK). This pilot study evaluates individual responses to pirfenidone, nintedanib and SFK inhibitor saracatinib, markers of redox homeostasis, fibrosis and inflammation, in IPF-derived human bronchial epithelial (HBE) cells. Differentiated HBE cells from patients with and without IPF were analyzed for potential alterations in redox and profibrotic genes and pro-inflammatory cytokine secretion. Additionally, the effects of pirfenidone, nintedanib and saracatinib on these markers were determined. HBE cells were differentiated into a bronchial epithelium containing ciliated epithelial, basal, goblet and club cells. NOX4 expression was increased in IPF-derived HBE cells but differed on an individual level. In patients with higher NOX4 expression, pirfenidone induced antioxidant gene expression. All drugs significantly decreased NOX4 expression. IL-6 (p = 0.09) and IL-8 secretion (p = 0.014) were increased in IPF-derived HBE cells and significantly reduced by saracatinib. Finally, saracatinib significantly decreased TGF-β gene expression. Our results indicate that treatment responsiveness varies between IPF patients in relation to their oxidative and inflammatory status. Interestingly, saracatinib tends to be more effective in IPF than standard antifibrotic drugs. Full article
(This article belongs to the Special Issue Redox Regulation in Pulmonary Diseases)
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18 pages, 3040 KiB  
Article
L-carnosine Attenuates Bleomycin-Induced Oxidative Stress via NFκB Pathway in the Pathogenesis of Pulmonary Fibrosis
by Jaehyun Park, Jimin Jang, Sang-Ryul Cha, Hyosin Baek, Jooyeon Lee, Seok-Ho Hong, Hyang-Ah Lee, Tae-Jin Lee and Se-Ran Yang
Antioxidants 2022, 11(12), 2462; https://doi.org/10.3390/antiox11122462 - 14 Dec 2022
Cited by 2 | Viewed by 2063
Abstract
Idiopathic Pulmonary fibrosis (IPF), a chronic interstitial lung disease, has pulmonary manifestations clinically characterized by collagen deposition, epithelial cell injury, and a decline in lung function. L-carnosine, a dipeptide consisting of β-alanine and L-histidine, has demonstrated a therapeutic effect on various diseases because [...] Read more.
Idiopathic Pulmonary fibrosis (IPF), a chronic interstitial lung disease, has pulmonary manifestations clinically characterized by collagen deposition, epithelial cell injury, and a decline in lung function. L-carnosine, a dipeptide consisting of β-alanine and L-histidine, has demonstrated a therapeutic effect on various diseases because of its pivotal function. Despite the effect of L-carnosine in experimental IPF mice, its anti-oxidative effect and associated intercellular pathway, particularly alveolar epithelial cells, remain unknown. Therefore, we demonstrated the anti-fibrotic and anti-inflammatory effects of L-carnosine via Reactive oxygen species (ROS) regulation in bleomycin (BLM)-induced IPF mice. The mice were intratracheally injected with BLM (3 mg/kg) and L-carnosine (150 mg/kg) was orally administrated for 2 weeks. BLM exposure increased the protein level of Nox2, Nox4, p53, and Caspase-3, whereas L-carnosine treatment suppressed the protein level of Nox2, Nox4, p53, and Caspase-3 cleavage in mice. In addition, the total SOD activity and mRNA level of Sod2, catalase, and Nqo1 increased in mice treated with L-carnosine. At the cellular level, a human fibroblast (MRC-5) and mouse alveolar epithelial cell (MLE-12) were exposed to TGFβ1 following L-carnosine treatment to induce fibrogenesis. Moreover, MLE-12 cells were exposed to cigarette smoke extract (CSE). Consequently, L-carnosine treatment ameliorated fibrogenesis in fibroblasts and alveolar epithelial cells, and inflammation induced by ROS and CSE exposure was ameliorated. These results were associated with the inhibition of the NFκB pathway. Collectively, our data indicate that L-carnosine induces anti-inflammatory and anti-fibrotic effects on alveolar epithelial cells against the pathogenesis of IPF. Full article
(This article belongs to the Special Issue Redox Regulation in Pulmonary Diseases)
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12 pages, 925 KiB  
Article
Oxidative Potential in Exhaled Air (OPEA) as a Tool for Predicting Certain Respiratory Disorders in the General Adult Population: Cross-Sectional Analysis Nested in the Swiss Health Study
by Irina Guseva Canu, Maud Hemmendinger, Antonio Toto, Pascal Wild, Caroline Veys-Takeuchi, Murielle Bochud and Guillaume Suárez
Antioxidants 2022, 11(10), 2079; https://doi.org/10.3390/antiox11102079 - 21 Oct 2022
Cited by 2 | Viewed by 1521
Abstract
In a pilot clinical study, OPEA allowed for distinguishing participants with and without chronic obstructive pulmonary disease. This study aimed to assess whether abnormal spirometry parameters and immunity against SARS-CoV-2 are associated with increased OPEA and estimating the OPEA reference interval. Swiss adult [...] Read more.
In a pilot clinical study, OPEA allowed for distinguishing participants with and without chronic obstructive pulmonary disease. This study aimed to assess whether abnormal spirometry parameters and immunity against SARS-CoV-2 are associated with increased OPEA and estimating the OPEA reference interval. Swiss adult residents of the Vaud Canton aged 20–69 years randomly selected from the Federal Statistical Office’s registries, speaking French or German, were included and examined between 1 October 2020 and 31 December 2021. General health status and presence of respiratory diseases were assessed by questionnaire and spirometry. Spirometric results were compared with the predicted values and their lower limits of norms of the Global Lung Function Initiative. SARS-CoV-2-seroprevalence was assessed using the Luminex-based test of IgG. Statistical analysis consisted of unilateral t-tests and ANOVA. Lower and upper limit of OPEA reference interval with associated 90%-confidence interval (90%CI) were estimated for the sub-sample of healthy adults by bootstrap, after excluding outliers. The study sample included 247 participants. SARS-CoV-2-seropositive participants and those with an obstructive syndrome had a significantly higher OPEA than seronegative and healthy participants. The estimated reference interval was: −0.0516 (90%CI = −0.0735; −0.0316); −0.0044 (90%CI = −0.0224; 0.0153). OPEA could predict inflammatory-based respiratory disorders, but needs further validation in different settings and for other pathologies. Full article
(This article belongs to the Special Issue Redox Regulation in Pulmonary Diseases)
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18 pages, 3293 KiB  
Article
NiONP-Induced Oxidative Stress and Mitochondrial Impairment in an In Vitro Pulmonary Vascular Cell Model Mimicking Endothelial Dysfunction
by Ophélie Germande, Thomas Ducret, Jean-Francois Quignard, Juliette Deweirdt, Véronique Freund-Michel, Marie-Hélène Errera, Guillaume Cardouat, Pierre Vacher, Bernard Muller, Patrick Berger, Christelle Guibert, Magalie Baudrimont and Isabelle Baudrimont
Antioxidants 2022, 11(5), 847; https://doi.org/10.3390/antiox11050847 - 26 Apr 2022
Cited by 3 | Viewed by 1937
Abstract
The development and use of nanomaterials, especially of nickel oxide nanoparticles (NiONPs), is expected to provide many benefits but also has raised concerns about the potential human health risks. Inhaled NPs are known to exert deleterious cardiovascular side effects, including pulmonary hypertension. Consequently, [...] Read more.
The development and use of nanomaterials, especially of nickel oxide nanoparticles (NiONPs), is expected to provide many benefits but also has raised concerns about the potential human health risks. Inhaled NPs are known to exert deleterious cardiovascular side effects, including pulmonary hypertension. Consequently, patients with pulmonary hypertension (PH) could be at increased risk for morbidity. The objective of this study was to compare the toxic effects of NiONPs on human pulmonary artery endothelial cells (HPAEC) under physiological and pathological conditions. The study was conducted with an in vitro model mimicking the endothelial dysfunction observed in PH. HPAEC were cultured under physiological (static and normoxic) or pathological (20% cycle stretch and hypoxia) conditions and exposed to NiONPs (0.5–5 μg/cm2) for 4 or 24 h. The following endpoints were studied: (i) ROS production using CM-H2DCF-DA and MitoSOX probes, (ii) nitrite production by the Griess reaction, (iii) IL-6 secretion by ELISA, (iv) calcium signaling with a Fluo-4 AM probe, and (v) mitochondrial dysfunction with TMRM and MitoTracker probes. Our results evidenced that under pathological conditions, ROS and nitrite production, IL-6 secretions, calcium signaling, and mitochondria alterations increased compared to physiological conditions. Human exposure to NiONPs may be associated with adverse effects in vulnerable populations with cardiovascular risks. Full article
(This article belongs to the Special Issue Redox Regulation in Pulmonary Diseases)
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12 pages, 1913 KiB  
Article
Role of Lung P450 Oxidoreductase in Paraquat-Induced Collagen Deposition in the Lung
by Nataliia Kovalchuk, Joseph L. Jilek, Laura S. Van Winkle, Nathan J. Cherrington and Xinxin Ding
Antioxidants 2022, 11(2), 219; https://doi.org/10.3390/antiox11020219 - 24 Jan 2022
Cited by 2 | Viewed by 2211
Abstract
Paraquat (PQ) is an agrochemical known to cause pulmonary fibrosis. PQ-induced collagen deposition in the lung is thought to require enzymatic formation of PQ radicals, but the specific enzymes responsible for this bioactivation event in vivo have not been identified. We tested the [...] Read more.
Paraquat (PQ) is an agrochemical known to cause pulmonary fibrosis. PQ-induced collagen deposition in the lung is thought to require enzymatic formation of PQ radicals, but the specific enzymes responsible for this bioactivation event in vivo have not been identified. We tested the hypothesis that lung P450 oxidoreductase (POR or CPR) is important in PQ-induced lung fibrosis in mice. A lung-Cpr-null mouse model was utilized, which undergoes doxycycline-induced, Cre recombinase-mediated deletion of the Por gene specifically in airway Club cells and alveolar type 2 cells in the lung. The lungs of lung-Cpr-null mice and their wild-type littermates were collected on day 15 after a single intraperitoneal injection of saline (control) or PQ (20 mg/kg). Lung tissue sections were stained with picrosirius red for detection of collagen fibrils. Fibrotic lung areas were found to be significantly smaller (1.6-fold for males and 1.4-fold for females) in PQ-treated lung-Cpr-null mice than in sex- and treatment-matched wild-type mice. The levels of collagen in lung tissue homogenate were also lower (1.4–2.3-fold; p < 0.05) in PQ-treated lung-Cpr-null mice compared to PQ-treated wild-type mice. In contrast, plasma PQ toxicokinetic profiles were not different between sex-matched wild-type and lung-Cpr-null mice. Taken together, these results indicate that lung POR plays an important role in PQ-induced pulmonary fibrosis. Full article
(This article belongs to the Special Issue Redox Regulation in Pulmonary Diseases)
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Review

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21 pages, 2885 KiB  
Review
Important Functions and Molecular Mechanisms of Mitochondrial Redox Signaling in Pulmonary Hypertension
by Jorge Reyes-García, Abril Carbajal-García, Annarita Di Mise, Yun-Min Zheng, Xiangdong Wang and Yong-Xiao Wang
Antioxidants 2022, 11(3), 473; https://doi.org/10.3390/antiox11030473 - 28 Feb 2022
Cited by 7 | Viewed by 3189
Abstract
Mitochondria are important organelles that act as a primary site to produce reactive oxygen species (ROS). Additionally, mitochondria play a pivotal role in the regulation of Ca2+ signaling, fatty acid oxidation, and ketone synthesis. Dysfunction of these signaling molecules leads to the [...] Read more.
Mitochondria are important organelles that act as a primary site to produce reactive oxygen species (ROS). Additionally, mitochondria play a pivotal role in the regulation of Ca2+ signaling, fatty acid oxidation, and ketone synthesis. Dysfunction of these signaling molecules leads to the development of pulmonary hypertension (PH), atherosclerosis, and other vascular diseases. Features of PH include vasoconstriction and pulmonary artery (PA) remodeling, which can result from abnormal proliferation, apoptosis, and migration of PA smooth muscle cells (PASMCs). These responses are mediated by increased Rieske iron–sulfur protein (RISP)-dependent mitochondrial ROS production and increased mitochondrial Ca2+ levels. Mitochondrial ROS and Ca2+ can both synergistically activate nuclear factor κB (NF-κB) to trigger inflammatory responses leading to PH, right ventricular failure, and death. Evidence suggests that increased mitochondrial ROS and Ca2+ signaling leads to abnormal synthesis of ketones, which play a critical role in the development of PH. In this review, we discuss some of the recent findings on the important interactive role and molecular mechanisms of mitochondrial ROS and Ca2+ in the development and progression of PH. We also address the contributions of NF-κB-dependent inflammatory responses and ketone-mediated oxidative stress due to abnormal regulation of mitochondrial ROS and Ca2+ signaling in PH. Full article
(This article belongs to the Special Issue Redox Regulation in Pulmonary Diseases)
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19 pages, 2204 KiB  
Review
The Emerging Role of Macrophages in Chronic Obstructive Pulmonary Disease: The Potential Impact of Oxidative Stress and Extracellular Vesicle on Macrophage Polarization and Function
by Mauro Finicelli, Filomena Anna Digilio, Umberto Galderisi and Gianfranco Peluso
Antioxidants 2022, 11(3), 464; https://doi.org/10.3390/antiox11030464 - 26 Feb 2022
Cited by 23 | Viewed by 3692
Abstract
Chronic obstructive pulmonary disease (COPD) is one of the most common airway diseases, and it is considered a major global health problem. Macrophages are the most representative immune cells in the respiratory tract, given their role in surveying airways, removing cellular debris, immune [...] Read more.
Chronic obstructive pulmonary disease (COPD) is one of the most common airway diseases, and it is considered a major global health problem. Macrophages are the most representative immune cells in the respiratory tract, given their role in surveying airways, removing cellular debris, immune surveillance, and resolving inflammation. Macrophages exert their functions by adopting phenotypical changes based on the stimuli they receive from the surrounding tissue. This plasticity is described as M1/M2 macrophage polarization, which consists of a strictly coordinated process leading to a difference in the expression of surface markers, the production of specific factors, and the execution of biological activities. This review focuses on the role played by macrophages in COPD and their implication in inflammatory and oxidative stress processes. Particular attention is on macrophage polarization, given macrophage plasticity is a key feature in COPD. We also discuss the regulatory influence of extracellular vesicles (EVs) in cell-to-cell communications. EV composition and cargo may influence many COPD-related aspects, including inflammation, tissue remodeling, and macrophage dysfunctions. These findings could be useful for better addressing the role of macrophages in the complex pathogenesis and outcomes of COPD. Full article
(This article belongs to the Special Issue Redox Regulation in Pulmonary Diseases)
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