ArticleNature communications2021
Disulfide disruption reverses mucus dysfunction in allergic airway disease.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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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Who cites it
46 citing papers in PubMed, 64 citations in OpenAlex.
- Micro/nanoscale bubble-mediated mucolytic conditioning of the lung model of cystic fibrosis enhances nanoparticle transport through the mucus.Biomaterials · 2026Article
- Airway mucus plugs in asthma and chronic obstructive pulmonary disease: pathobiology, imaging, and implications for clinical trials.American journal of respiratory and critical care medicine · 2026Review
- Clearing the Pulmonary Traffic Jam With Dual-Enzyme Inhalable Nanoparticles Restore Airflow and Reverse Fibrotic Remodeling.Advanced healthcare materials · 2026Article
- Unraveling Oral Fate of Poly(Lipoic Acid)s: Mechanistic Insights and Delivery Horizons.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- 3D CT-Based quantification of airway structural changes during asthma exacerbations: a retrospective observational study.BMC pulmonary medicine · 2026Observational
- Aerodynamic barriers to inhaled furosemide delivery during dyspnoea revealed by experimental and computational modelling.Scientific reports · 2026Article
- Review
- Progress in treating mucus plugs in asthma.American journal of respiratory and critical care medicine · 2026Article
- Mechanically induced dysregulation of calcium homeostasis: a molecular linchpin in asthmatic pathogenesis.European journal of medical research · 2025Review
- Macroheterogeneities Induced by Disulfide Bond Reduction in Native Mucus.ACS applied bio materials · 2025Article
- Parasympathetic Airway Hyperreactivity Is Enhanced in Acute but Not Chronic Eosinophilic Asthma Mouse Models.American journal of respiratory cell and molecular biology · 2025Article
- Global scenario of silica-associated diseases: A review on emerging pathophysiology of silicosis and potential therapeutic regimes.Toxicology reports · 2025Review
- Mucins and Their Roles in Asthma.Immunological reviews · 2025Review
- Hydrogen-induced disruption of the airway mucus barrier enhances nebulized RNA delivery to reverse pulmonary fibrosis.Science advances · 2025Article
- Requirement for Fucosyltransferase 2 in Allergic Airway Hyperreactivity and Mucus Obstruction.American journal of respiratory cell and molecular biology · 2025Article
- High-throughput Mucus Microrheology for Phenotyping and Disease Modeling.bioRxiv : the preprint server for biology · 2025Article
- The Tmem16a chloride channel is required for mucin maturation after secretion from goblet-like cells in the Xenopus tropicalis tadpole skin.Scientific reports · 2024Article
- Mucociliary clearance is impaired in small airways of cystic fibrosis pigs.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Emerging cell and molecular targets for treating mucus hypersecretion in asthma.Allergology international : official journal of the Japanese Society of Allergology · 2024Review
- Synthetic mucus barrier arrays as a nanoparticle formulation screening platform.RSC pharmaceutics · 2024Article
Corrections and comments
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Authors and funding
21 authors at 7 institutions in 2 countries.
Funding
Abstract
Airway mucus is essential for lung defense, but excessive mucus in asthma obstructs airflow, leading to severe and potentially fatal outcomes. Current asthma treatments have minimal effects on mucus, and the lack of therapeutic options stems from a poor understanding of mucus function and dysfunction at a molecular level and in vivo. Biophysical properties of mucus are controlled by mucin glycoproteins that polymerize covalently via disulfide bonds. Once secreted, mucin glycopolymers can aggregate, form plugs, and block airflow. Here we show that reducing mucin disulfide bonds disrupts mucus in human asthmatics and reverses pathological effects of mucus hypersecretion in a mouse allergic asthma model. In mice, inhaled mucolytic treatment loosens mucus mesh, enhances mucociliary clearance, and abolishes airway hyperreactivity (AHR) to the bronchoprovocative agent methacholine. AHR reversal is directly related to reduced mucus plugging. These findings establish grounds for developing treatments to inhibit effects of mucus hypersecretion 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.