ArticlePloS one2013
S-nitrosoglutathione reductase inhibition regulates allergen-induced lung inflammation and airway hyperreactivity.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Effect of the S-nitrosoglutathione reductase inhibitor N6022 on bronchial hyperreactivity in asthma.Immunity, inflammation and disease · 2018Trial
- Pharmacologic Inhibition of S-Nitrosoglutathione Reductase Prevents Hyperoxic Alveolar and Airway Disease in Newborn Mice.Biomedicines · 2025Article
- Mycothiol maintains the homeostasis and signalling of nitric oxide in Streptomyces coelicolor A3(2) M145.BMC microbiology · 2023Article
- Exploring redox imbalance and inflammation for asthma therapy.Molecular biology reports · 2023Review
- Protein S-Nitrosylation: Determinants of Specificity and Enzymatic Regulation of S-Nitrosothiol-Based Signaling.Antioxidants & redox signaling · 2019Review
- Identification of a Novel Inhibitor of Human Rhinovirus Replication and Inflammation in Airway Epithelial Cells.American journal of respiratory cell and molecular biology · 2019Article
- GSNOR modulates hyperhomocysteinemia-induced T cell activation and atherosclerosis by switching Akt S-nitrosylation to phosphorylation.Redox biology · 2018Article
- Winner of the society for biomaterials young investigator award for the annual meeting of the society for biomaterials, April 11-14, 2018, Atlanta, GA: S-nitrosated poly(propylene sulfide) nanoparticles for enhanced nitric oxide delivery to lymphatic tissues.Journal of biomedical materials research. Part A · 2018Article
- S-nitrosoglutathione reductase (GSNOR) inhibitor as an immune modulator in experimental autoimmune encephalomyelitis.Free radical biology & medicine · 2018Article
- S-Nitrosoglutathione Reductase Underlies the Dysfunctional Relaxation to Nitric Oxide in Preterm Labor.Scientific reports · 2018Article
- Prenatal environmental tobacco smoke exposure increases allergic asthma risk with methylation changes in mice.Environmental and molecular mutagenesis · 2017Article
- The role of S-nitrosoglutathione reductase (GSNOR) in human disease and therapy.Critical reviews in biochemistry and molecular biology · 2017Review
- Hypoxia inducible factor-1 alpha stabilization for regenerative therapy in traumatic brain injury.Neural regeneration research · 2017Review
- Recent developments in the role of reactive oxygen species in allergic asthma.Journal of thoracic disease · 2017Review
- S-Nitrosoglutathione Attenuates Airway Hyperresponsiveness in Murine Bronchopulmonary Dysplasia.Molecular pharmacology · 2016Article
- Chinese expert consensus on clinical use of non-invasive airway inflammation assessment in bronchial asthma.Journal of thoracic disease · 2015Review
- Chinese expert consensus on clinical use of non-invasive airway inflammation assessment in bronchial asthma.Annals of translational medicine · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Allergic asthma is characterized by Th2 type inflammation, leading to airway hyperresponsivenes, mucus hypersecretion and tissue remodeling. S-Nitrosoglutathione reductase (GSNOR) is an alcohol dehydrogenase involved in the regulation of intracellular levels of S-nitrosothiols. GSNOR activity has been shown to be elevated in human asthmatic lungs, resulting in diminished S-nitrosothiols and thus contributing to increased airway hyperreactivity. Using a mouse model of allergic airway inflammation, we report that intranasal administration of a new selective inhibitor of GSNOR, SPL-334, caused a marked reduction in airway hyperreactivity, allergen-specific T cells and eosinophil accumulation, and mucus production in the lungs in response to allergen inhalation. Moreover, SPL-334 treatment resulted in a significant decrease in the production of the Th2 cytokines IL-5 and IL-13 and the level of the chemokine CCL11 (eotaxin-1) in the airways. Collectively, these observations reveal that GSNOR inhibitors are effective not only in reducing airway hyperresponsiveness but also in limiting lung inflammatory responses mediated by CD4(+) Th2 cells. These findings suggest that the inhibition of GSNOR may provide a novel therapeutic approach for the treatment of allergic airway inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.