ArticleNature communications2018
Muc5b overexpression causes mucociliary dysfunction and enhances lung fibrosis in mice.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers, 3 of them syntheses that pooled it.
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
168 citing papers in PubMed, 3 syntheses or guidelines pooled it, 236 citations in OpenAlex.
- Molecular Systems Architecture of Fibrotic Lung Microenvironment in Idiopathic Pulmonary Fibrosis.Cells · 2026Pooled it
- Emodin for pulmonary fibrosis: a systematic review and meta-analysis of efficacy and molecular mechanisms.Frontiers in medicine · 2025Pooled it
- Mammalian Neuraminidases in Immune-Mediated Diseases: Mucins and Beyond.Frontiers in immunology · 2022Pooled it
- Detergent-Containing Toothpaste Decreases Esophageal Mucosal Impedance and Alters Salivary Properties in Humans.Allergy · 2026Article
- What Explains the Pattern of Fibrosis in Chronic Graft-Versus-Host Disease?Clinical transplantation · 2026Review
- Clearing the Pulmonary Traffic Jam With Dual-Enzyme Inhalable Nanoparticles Restore Airflow and Reverse Fibrotic Remodeling.Advanced healthcare materials · 2026Article
- Telomere dysfunction and mucociliary impairment drive idiopathic pulmonary fibrosis susceptibility: insights from a Sardinian whole-exome study.BMJ open respiratory research · 2026Article
- A SNP altering the MUC5AC mucin structure is increased in idiopathic pulmonary fibrosis together with the MUC5B SNP.Respiratory research · 2026Article
- Airway secretory cells contain both a perinuclear Golgi ribbon and dispersed Golgi satellites.American journal of respiratory cell and molecular biology · 2026Article
- Beyond scarring: a next-generation vision for pulmonary fibrosis management.Molecular biology reports · 2026Review
- Recent advances in pulmonary fibrosis: from lung surfactant to the immune connection.Respiratory research · 2026Review
- Causal and shared genetic insights into severe COVID-19 and idiopathic pulmonary fibrosis.iScience · 2026Article
- Genes, other than Muc5b, are associated with bleomycin-induced lung injury.Communications biology · 2026Article
- Ectopic expression of MUC5B in the respiratory bronchiole initiates endoplasmic reticulum stress in the IPF lung.American journal of respiratory cell and molecular biology · 2026Article
- Interferon-γ selectively promotes survival of alveolar progenitor cells in a human lung organoid model.The EMBO journal · 2026Article
- Inactivating conditions of therapeutic mycobacteriophages.Microbiology spectrum · 2026Article
- Research progress on the mechanisms of mucus retention after mycoplasma pneumoniae infection.Frontiers in cellular and infection microbiology · 2026Review
- YF Reduces Alveolar Epithelial Cell Apoptosis and PF by Inactivating JAK2/STAT3.Current pharmaceutical design · 2026Article
- Epigenomic study of the lower airway reveals COPD-associated methylation patterns and potential microbiota links.BMJ open respiratory research · 2025Article
- Insight into the pathogenesis of interstitial lung diseases and near-to-native lung fibrosis models.European journal of medical research · 2025Review
108 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
20 authors at 7 institutions in 1 country.
Funding
Abstract
The gain-of-function MUC5B promoter variant rs35705950 is the dominant risk factor for developing idiopathic pulmonary fibrosis (IPF). Here we show in humans that MUC5B, a mucin thought to be restricted to conducting airways, is co-expressed with surfactant protein C (SFTPC) in type 2 alveolar epithelia and in epithelial cells lining honeycomb cysts, indicating that cell types involved in lung fibrosis in distal airspace express MUC5B. In mice, we demonstrate that Muc5b concentration in bronchoalveolar epithelia is related to impaired mucociliary clearance (MCC) and to the extent and persistence of bleomycin-induced lung fibrosis. We also establish the ability of the mucolytic agent P-2119 to restore MCC and to suppress bleomycin-induced lung fibrosis in the setting of Muc5b overexpression. Our findings suggest that mucociliary dysfunction might play a causative role in bleomycin-induced pulmonary fibrosis in mice overexpressing Muc5b, and that MUC5B in distal airspaces is a potential therapeutic target in humans with IPF.
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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.