ReviewChinese medical journal pulmonary and critical care medicine2026
Structural and cellular mechanisms of mucus plugging in the larger airways.
Review in Chinese medical journal pulmonary and critical care medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Prediction of Prolonged Length of Hospital Stay in Patients with Acute Exacerbations of Chronic Obstructive Pulmonary Disease: An Interpretable Machine Learning Tool.Journal of clinical medicine · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intractable mucus plugging drives mortality in cystic fibrosis (CF), asthma, and chronic obstructive pulmonary disease (COPD). While surface metaplasia narrows small airways, the massive volumetric reservoir capacity of hypertrophied submucosal glands (SMGs) dictates catastrophic mucus plugging in the larger airways. This review proposes a flush-load model to explain this structural failure: a biophysical imbalance in which SMG serous fluid secretion (the flush) is insufficient to hydrate and clear the burden of high-molecular-weight mucins (the load), leading to osmotic compression, ciliary collapse, and intractable luminal occlusion. The review delineates the disease-specific etiologies of this imbalance. In CF, dysfunction of ion channels, such as the cystic fibrosis transmembrane conductance regulator (CFTR) and epithelial sodium channels (ENaC), causes mechanical uncoupling and mucin 5B (MUC5B) tethering to glandular ducts. In asthma, Type 2 inflammation disrupts the glandular stem cells, driving an explosive release of mucin. In COPD, epidermal growth factor receptor (EGFR)-driven remodeling and senescent inflammaging perpetuate chronic hypersecretion. Ultimately, anchored MUC5B strands from hypertrophic SMGs structurally integrate with surface-derived mucin 5AC (MUC5AC), forming an intractable adhesive mesh. Synthesizing these insights, we advocate shifting the therapeutic paradigm from symptomatic downstream clearance to upstream, disease-modifying interventions that target the glandular stem cell niche, restore ion channel homeostasis, and correct coordinated airway surface dysfunction.
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