ReviewCurrent opinion in pulmonary medicine2009
Mucus hypersecretion in asthma: causes and effects.
Review in Current opinion in pulmonary medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
154 citing papers in PubMed, 281 citations in OpenAlex.
- Effect of inhaled dust mite allergen on regional particle deposition and mucociliary clearance in allergic asthmatics.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2011Trial
- Sphingomyelin synthase 2 deficiency suppresses airway mucus accumulation by altering sphingolipid flux and mucin glycosylation.Molecular and cellular biochemistry · 2026Article
- MUC5B and MUC5AC function in combination to regulate mucociliary transport on human airway epithelium.bioRxiv : the preprint server for biology · 2026Article
- 3D CT-Based quantification of airway structural changes during asthma exacerbations: a retrospective observational study.BMC pulmonary medicine · 2026Observational
- Structural and cellular mechanisms of mucus plugging in the larger airways.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Functional Variant Discovery Identifies a Novel Genetic Link between SPRY2, Wood Smoke, and Asthma.American journal of respiratory cell and molecular biology · 2026Article
- Boron Nitride Nanomaterials Trigger Immunomodulatory Effects in Human Broncho-Epithelial Cells by Modulating Eicosanoid Lipid Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Verteporfin, an inhibitor of nuclear YAP, improved multi-ciliated cell differentiation in the airway epithelium.Journal of translational medicine · 2025Article
- Smart Inhalation Therapy: Boosting siRNA Efficacy with Inulin-Based Multifunctional Polymers.ACS applied materials & interfaces · 2025Article
- Article
- Combustion products of burn pit constituents induce more changes in asthmatic than non-asthmatic murine lungs.Particle and fibre toxicology · 2025Article
- BRL-50481 Ameliorates Lung Inflammation in a Murine Model of Ovalbumin-Induced Allergic Asthma with Co-Exposure to Lipopolysaccharide.Biomolecules & therapeutics · 2025Article
- Hederacoside C Modulates EGF-Induced MUC5AC Mucin Gene Expression by Regulating the MAPK Signaling Pathway in Human Airway Epithelial Cells.Biomolecules & therapeutics · 2025Article
- Pharmacological inhibition of MutT homolog 1 (MTH1) in allergic airway inflammation as a novel treatment strategy.Respiratory research · 2025Article
- Physiology and pathophysiology of mucus and mucolytic use in critically ill patients.Critical care (London, England) · 2025Review
- Characteristics ofFrontiers in immunology · 2025Article
- Promoting immune defensive responses of epithelial cells in airway disease.Frontiers in allergy · 2025Review
- Therapeutic effects of a combination ofFrontiers in nutrition · 2025Article
- The Link Between Dysbiosis, Inflammation, Oxidative Stress, and Asthma-The Role of Probiotics, Prebiotics, and Antioxidants.Nutrients · 2024Review
- Emodin Inhibited MUC5AC Mucin Gene Expression via Affecting EGFR-MAPK-Sp1 Signaling Pathway in Human Airway Epithelial Cells.Biomolecules & therapeutics · 2024Article
94 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
purpose of reviewAirway mucus plugging has long been recognized as a principal cause of death in asthma. However, molecular mechanisms of mucin overproduction and secretion have not been understood until recently. These mechanisms are reviewed together with ongoing investigations relating them to lung pathophysiology. RECENT
findingsOf the five secreted gel-forming mucins in mammals, only MUC5AC and MUC5B are produced in significant quantities in intrapulmonary airways. MUC5B is the principal gel-forming mucin at baseline in small airways of humans and mice, and therefore likely performs most homeostatic clearance functions. MUC5AC is the principal gel-forming mucin upregulated in airway inflammation and is under negative control by forkhead box a2 (Foxa2) and positive control by hypoxia inducible factor-1 (HIF-1). Mucin secretion is regulated separately from production, principally by extracellular triphosphate nucleotides that bind P2Y2 receptors on the lumenal surface of airway secretory cells, generating intracellular second messengers that activate the exocytic proteins, Munc13-2 and synaptotagmin-2. SUMMARY: Markedly upregulated production of MUC5AC together with stimulated secretion leads to airflow obstruction in asthma. As MUC5B appears to mediate homeostatic functions, it may be possible to selectively inhibit MUC5AC production without impairing airway function. The precise roles of mucin hypersecretion in asthma symptoms such as dyspnea and cough and in physiologic phenomena such as airway hyperresponsiveness remain to be defined.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.