ArticleAmerican journal of respiratory cell and molecular biology2017
Superoxide Dismutase 3 R213G Single-Nucleotide Polymorphism Blocks Murine Bleomycin-Induced Fibrosis and Promotes Resolution of Inflammation.
Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- R213G-Mediated Redistribution of EC-SOD Protects Against Sugen-Hypoxia Pulmonary Hypertension in Mice.Pulmonary circulation · 2026Article
- Deacetylation of SOD3 by sirtuins restores furin cleavage.Redox biochemistry and chemistry · 2025Article
- Redistribution of SOD3 expression due to R213G polymorphism affects pulmonary interstitial macrophage reprogramming in response to hypoxia.Physiological genomics · 2024Article
- Lung EC-SOD Overexpression Prevents Hypoxia-Induced Platelet Activation and Lung Platelet Accumulation.Antioxidants (Basel, Switzerland) · 2024Article
- Release of extracellular superoxide dismutase into alveolar fluid protects against acute lung injury and inflammation inAmerican journal of physiology. Lung cellular and molecular physiology · 2023Article
- Pharmacology and Emerging Therapies for Group 3 Pulmonary Hypertension Due to Chronic Lung Disease.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Potential Role of Superoxide Dismutase 3 (SOD3) in Resistance to Influenza A Virus Infection.Antioxidants (Basel, Switzerland) · 2023Article
- Extracellular superoxide dismutase (EC-SOD) R213G variant reduces mitochondrial ROS and preserves mitochondrial function in bleomycin-induced lung injury: EC-SOD R213G variant and intracellular redox regulation.Advances in redox research · 2022Article
- Airway Redox Homeostasis and Inflammation Gone Awry: From Molecular Pathogenesis to Emerging Therapeutics in Respiratory Pathology.International journal of molecular sciences · 2020Review
- MicroRNA regulation postbleomycin due to the R213G extracellular superoxide dismutase variant is predicted to suppress inflammatory and immune pathways.Physiological genomics · 2020Article
- Extracellular superoxide dismutase, a molecular transducer of health benefits of exercise.Redox biology · 2020Review
- MyD88 regulates a prolonged adaptation response to environmental dust exposure-induced lung disease.Respiratory research · 2020Article
- Anti-oxidative effects of superoxide dismutase 3 on inflammatory diseases.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Redistribution of EC-SOD resolves bleomycin-induced inflammationFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Acute and chronic changes in the control of breathing in a rat model of bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Oxidative Toxicology of Bleomycin: Role of the Extracellular Redox Environment.Current opinion in toxicology · 2019Article
- Use of Electron Paramagnetic Resonance in Biological Samples at Ambient Temperature and 77 K.Journal of visualized experiments : JoVE · 2019Article
- Role of SOD3 in silica-related lung fibrosis and pulmonary vascular remodeling.Respiratory research · 2018Article
- MicroRNA dysregulation in lung injury: the role of the miR-26a/EphA2 axis in regulation of endothelial permeability.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- R213G polymorphism in SOD3 protects against bleomycin-induced inflammation and attenuates induction of proinflammatory pathways.Physiological genomics · 2018Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Loss of extracellular superoxide dismutase 3 (SOD3) contributes to inflammatory and fibrotic lung diseases. The human SOD3 R213G polymorphism decreases matrix binding, redistributing SOD3 from the lung to extracellular fluids, and protects against LPS-induced alveolar inflammation. We used R213G mice expressing a naturally occurring single-nucleotide polymorphism, rs1799895, within the heparin-binding domain of SOD3, which results in an amino acid substitution at position 213 to test the hypothesis that the redistribution of SOD3 into the extracellular fluids would impart protection against bleomycin-induced lung fibrosis and secondary pulmonary hypertension (PH). In R213G mice, SOD3 content and activity was increased in extracellular fluids and decreased in lung at baseline, with greater increases in bronchoalveolar lavage fluid (BALF) SOD3 compared with wild-type mice 3 days after bleomycin. R213G mice developed less fibrosis based on pulmonary mechanics, fibrosis scoring, collagen quantification, and gene expression at 21 days, and less PH by right ventricular systolic pressure and pulmonary arteriole medial wall thickening at 28 days. In wild-type mice, macrophages, lymphocytes, neutrophils, proinflammatory cytokines, and protein increased in BALF on Day 7 and/or 21. In R213G mice, total BALF cell counts increased on Day 7 but resolved by 21 days. At 1 or 3 days, BALF pro- and antiinflammatory cytokines and BALF protein were higher in R213G mice, resolving by 21 days. We conclude that the redistribution of SOD3 as a result of the R213G single-nucleotide polymorphism protects mice from bleomycin-induced fibrosis and secondary PH by improved resolution of alveolar inflammation.
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