Oxidative Stress in Lung 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 December 2024 | Viewed by 887

Special Issue Editor


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Guest Editor
Vascular Biology Center, Division of Pulmonary Critical Care Medicine, Medical College of Georgia, Augusta University, 1460, Laney-Walker Blvd, Augusta, GA 30912, USA
Interests: pneumonia; pulmonary edema; TNF; epithelial sodium channel; pneumolysin
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Special Issue Information

Dear Colleagues,

Oxidative stress plays a pivotal role in both the host defense mechanisms and the pathogenesis and progression of lung injury caused by bacterial, viral or fungal pathogens. This Special Issue "Oxidative Stress in Lung Diseases" aims to explore the intricate mechanisms by which oxidative stress contributes to pulmonary pathology as well as to immune defense mechanisms and to highlight potential therapeutic interventions.

We invite submissions that focus on the molecular and cellular mechanisms by which oxidative stress influences lung diseases. Topics of interest include, but are not limited to, the following:

  • Mechanisms of Oxidative Damage: Investigations into how reactive oxygen species (ROS) and reactive nitrogen species (RNS) generated by pathogens or by host immune cells cause cellular and tissue damage in lung diseases such as pneumonia, ARDS, chronic obstructive pulmonary disease (COPD), asthma, idiopathic pulmonary fibrosis (IPF), and lung cancer.
  • Antioxidant Defense Systems: Studies on the role of endogenous antioxidants and the therapeutic potential of antioxidant supplementation in mitigating oxidative stress-related lung damage.
  • Inflammatory Responses: Research on the interplay between oxidative stress and inflammation, and how this contributes to disease progression and exacerbation in respiratory conditions.
  • Biomarkers of Oxidative Stress: Identification and validation of biomarkers for early detection, prognosis, and monitoring of lung diseases accompanied by oxidative stress.
  • Therapeutic Approaches: Development and evaluation of novel antioxidants and pharmacological interventions aimed at reducing oxidative stress in lung diseases.
  • Environmental and Lifestyle Factors: Analysis of how external factors, such as air pollution, smoking, and diet, influence oxidative stress and lung health.

We welcome original research articles, reviews, and clinical studies that provide insights into oxidative stress mechanisms, novel therapeutic targets, and interventions in the context of lung diseases. This Special Issue aims to foster a comprehensive understanding of oxidative stress in lung diseases and promote the development of innovative treatments to enhance respiratory health.

Prof. Dr. Rudolf Lucas
Guest Editor

Manuscript Submission Information

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Keywords

  • ROS
  • RNS
  • lung diseases
  • antioxidant defense
  • respiratory health

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Published Papers (1 paper)

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Research

10 pages, 5405 KiB  
Communication
Loss of Surfactant Protein A Alters Perinatal Lung Morphology and Susceptibility to Hyperoxia-Induced Bronchopulmonary Dysplasia
by Shaili Amatya, Matthew Lanza, Todd M. Umstead and Zissis C. Chroneos
Antioxidants 2024, 13(11), 1309; https://doi.org/10.3390/antiox13111309 - 28 Oct 2024
Viewed by 649
Abstract
Bronchopulmonary dysplasia (BPD) is a condition of poor alveolar formation that causes chronic breathing impairment in infants born prematurely. Preterm lungs lack surfactant and are vulnerable to oxidative injuries driving the development of BPD. Our recent studies reported that surfactant protein A (SP-A) [...] Read more.
Bronchopulmonary dysplasia (BPD) is a condition of poor alveolar formation that causes chronic breathing impairment in infants born prematurely. Preterm lungs lack surfactant and are vulnerable to oxidative injuries driving the development of BPD. Our recent studies reported that surfactant protein A (SP-A) genetic variants influence susceptibility to neonatal lung disease. SP-A modulates activation of alveolar macrophages and parturition onset in late gestation. We asked whether a lack of SP-A alters alveolarization in a mouse model of hyperoxia-induced BPD. SP-A-deficient and control newborn mice were exposed to either clinically relevant 60% O2 hyperoxia or normoxia for 5–7 days. Alveolar formation was then assessed by mean linear intercept (MLI) and radial alveolar count (RAC) measurements in lung tissue sections. We report that the combination of SP-A deficiency and hyperoxia reduces alveolar growth compared to WT mice. The morphometric analysis of normoxic SP-A-deficient lungs showed lower RAC compared to controls, indicating reduced alveolar number. In the presence of hyperoxia, MLI was higher in SP-A-deficient lungs compared to controls. Differences were statistically significant for female pups. Spatial proteomic profiling of lung tissue sections showed that hyperoxia caused a 4-fold increase in the DNA damage marker γH2Ax in macrophages of SP-A-deficient lungs compared to normoxia. Our short report suggests an important role for SP-A in perinatal lung development and the protection of lung macrophages from oxidant injury. These studies warrant future investigation to discern the temporal interaction of SP-A, gender, oxidant injury, and lung macrophages in perinatal alveolar formation and development of BPD. Full article
(This article belongs to the Special Issue Oxidative Stress in Lung Diseases)
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