ArticleScience translational medicine2013
CaMKII is essential for the proasthmatic effects of oxidation.
Article in Science translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
The trial behind it
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
45 citing papers in PubMed, 63 citations in OpenAlex.
- Review
- LRRC8A drives NADPH oxidase-mediated mitochondrial dysfunction and inflammation in allergic rhinitis.Journal of translational medicine · 2024Article
- PKM2 regulates metabolic flux and oxidative stress in the murine heart.Physiological reports · 2024Article
- TRPM2 exacerbates airway inflammation by regulating oxidized-CaMKⅡ in allergic asthma.Heliyon · 2024Article
- Autophagy/Mitophagy in Airway Diseases: Impact of Oxidative Stress on Epithelial Cells.Biomolecules · 2023Review
- Selection and validation of genes related to oxidative stress production and clearance in macrophages infected withFrontiers in cellular and infection microbiology · 2023Article
- Overview of the Mechanisms of Oxidative Stress: Impact in Inflammation of the Airway Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Wnt 5a mediated inflammatory injury of renal tubular epithelial cells dependent on calcium signaling pathway in Trichloroethylene sensitized mice.Ecotoxicology and environmental safety · 2022Article
- Activation of cannabinoid receptor 2 attenuates Angiotensin II-induced atrial fibrillationFrontiers in cardiovascular medicine · 2022Article
- CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution.Nature communications · 2021Article
- CaMKII oxidation regulates cockroach allergen-induced mitophagy in asthma.The Journal of allergy and clinical immunology · 2021Article
- Mitochondria in Focus: From Function to Therapeutic Strategies in Chronic Lung Diseases.Frontiers in immunology · 2021Review
- Epithelial Aryl Hydrocarbon Receptor Protects From Mucus Production by Inhibiting ROS-Triggered NLRP3 Inflammasome in Asthma.Frontiers in immunology · 2021Article
- Inhibition of CaMKII in mitochondria preserves endothelial barrier function after irradiation.Free radical biology & medicine · 2020Article
- Article
- Inhibitor 1 of Protein Phosphatase 1 Regulates CaOxidative medicine and cellular longevity · 2019Article
- Environmental Exposures and Asthma Development: Autophagy, Mitophagy, and Cellular Senescence.Frontiers in immunology · 2019Review
- Novel eosinophilic gene expression networks associated with IgE in two distinct asthma populations.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2018Article
- Oxidative stress in chronic lung disease: From mitochondrial dysfunction to dysregulated redox signaling.Molecular aspects of medicine · 2018Review
- The vagal ganglia transcriptome identifies candidate therapeutics for airway hyperreactivity.American journal of physiology. Lung cellular and molecular physiology · 2018Article
Corrections and comments
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Authors and funding
29 authors at 5 institutions in 1 country.
Funding
Abstract
Increased reactive oxygen species (ROS) contribute to asthma, but little is known about the molecular mechanisms connecting increased ROS with characteristic features of asthma. We show that enhanced oxidative activation of the Ca(2+)/calmodulin-dependent protein kinase (ox-CaMKII) in bronchial epithelium positively correlates with asthma severity and that epithelial ox-CaMKII increases in response to inhaled allergens in patients. We used mouse models of allergic airway disease induced by ovalbumin (OVA) or Aspergillus fumigatus (Asp) and found that bronchial epithelial ox-CaMKII was required to increase a ROS- and picrotoxin-sensitive Cl(-) current (ICl) and MUC5AC expression, upstream events in asthma progression. Allergen challenge increased epithelial ROS by activating NADPH oxidases. Mice lacking functional NADPH oxidases due to knockout of p47 and mice with epithelial-targeted transgenic expression of a CaMKII inhibitory peptide or wild-type mice treated with inhaled KN-93, an experimental small-molecule CaMKII antagonist, were protected against increases in ICl, MUC5AC expression, and airway hyperreactivity to inhaled methacholine. Our findings support the view that CaMKII is a ROS-responsive, pluripotent proasthmatic signal and provide proof-of-concept evidence that CaMKII is a therapeutic target in asthma.
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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.