ArticleAmerican journal of respiratory and critical care medicine2009
NADPH oxidase-1 plays a crucial role in hyperoxia-induced acute lung injury in mice.
Article in American journal of respiratory and critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Who cites it
104 citing papers in PubMed, 163 citations in OpenAlex.
- Vitamin D to Prevent Lung Injury Following Esophagectomy-A Randomized, Placebo-Controlled Trial.Critical care medicine · 2018Trial
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- EphA2 monoclonal antibody attenuates hyperoxia-induced acute lung injury by preserving the alveolar-endothelial barrier.Scientific reports · 2026Article
- RNA Sequencing Reveals Inflammatory and Metabolic Changes in the Lung and Brain After Carbon Black and Naphthalene Whole Body Inhalation Exposure in a Rodent Model of Military Burn Pit Exposures.International journal of molecular sciences · 2025Article
- Article
- Can ENaC "TIP" the Scales to Reduce Endothelial Reactive Oxygen Species and Vascular Leak during Pneumococcal Lung Injury?American journal of respiratory cell and molecular biology · 2025Article
- Endothelial ENaC-α Restrains Oxidative Stress in Lung Capillaries in Murine Pneumococcal Pneumonia-associated Acute Lung Injury.American journal of respiratory cell and molecular biology · 2025Article
- Oxidative stress in pediatric diseases associated with the origin of life and growth and development.Frontiers in cell and developmental biology · 2025Review
- Decoding STAT3: a new frontier in understanding and treating hyperoxic lung injury.Frontiers in immunology · 2025Review
- Research progress of mitochondrial dysfunction induced pyroptosis in acute lung injury.Respiratory research · 2024Review
- Use of Optical Redox Imaging to Quantify Alveolar Macrophage Redox State in Infants: Proof of Concept Experiments in a Murine Model and Human Tracheal Aspirates Samples.Antioxidants (Basel, Switzerland) · 2024Article
- Modified Qing-Zao-Jiu-Fei decoction attenuated pulmonary fibrosis induced by bleomycin in rats via modulating Nrf2/NF-κB and MAPKs pathways.Chinese medicine · 2024Article
- NOX-2 Inhibitors may be Potential Drug Candidates for the Management of COVID-19 Complications.Current drug research reviews · 2024Review
- Targeting oxidative stress as a preventive and therapeutic approach for cardiovascular disease.Journal of translational medicine · 2023Review
- Oxygen for the Newborn: Friend or Foe?Children (Basel, Switzerland) · 2023Review
- Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries.Antioxidants (Basel, Switzerland) · 2023Review
- Pre-clinical evidence of a dual NADPH oxidase 1/4 inhibitor (setanaxib) in liver, kidney and lung fibrosis.Journal of cellular and molecular medicine · 2023Review
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- Modulation of innate immunity in airway epithelium for host-directed therapy.Frontiers in immunology · 2023Review
- MERS-CoV nsp1 impairs the cellular metabolic processes by selectively downregulating mRNAs in a novel granules.Virulence · 2022Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
Abstract
rationaleHyperoxia-induced acute lung injury has been used for many years as a model of oxidative stress mimicking clinical acute lung injury and the acute respiratory distress syndrome. Excess quantities of reactive oxygen species (ROS) are responsible for oxidative stress-induced lung injury. ROS are produced by mitochondrial chain transport, but also by NADPH oxidase (NOX) family members. Although NOX1 and NOX2 are expressed in the lungs, their precise function has not been determined until now.
objectivesTo determine whether NOX1 and NOX2 contribute in vivo to hyperoxia-induced acute lung injury.
methodsWild-type and NOX1- and NOX2-deficient mice, as well as primary lung epithelial and endothelial cells, were exposed to room air or 100% O(2) for 72 hours. MEASUREMENTS AND MAIN
resultsLung injury was significantly prevented in NOX1-deficient mice, but not in NOX2-deficient mice. Hyperoxia-dependent ROS production was strongly reduced in lung sections, in isolated epithelial type II cells, and lung endothelial cells from NOX1-deficient mice. Concomitantly, lung cell death in situ and in primary cells was markedly decreased in NOX1-deficient mice. In wild-type mice, hyperoxia led to phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK), two mitogen-activated protein kinases involved in cell death signaling, and to caspase-3 activation. In NOX1-deficient mice, JNK phosphorylation was blunted, and ERK phosphorylation and caspase-3 activation were decreased.
conclusionsNOX1 is an important contributor to ROS production and cell death of the alveolocapillary barrier during hyperoxia and is an upstream actor in oxidative stress-induced acute lung injury involving JNK and ERK pathways in mice.
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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.