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Structural and cellular mechanisms of airway mucus plugging in the larger airways
Journal article   Open access   Peer reviewed

Structural and cellular mechanisms of airway mucus plugging in the larger airways

Zheqing Hu, Liyuan Yang, Yabo Ma, Juan Chen and Xiaoming Liu
Chinese medical journal pulmonary and critical care medicine, Vol.4(2)
06/10/2026
DOI: 10.1016/j.pccm.2026.05.001
PMID: 42396192
url
https://doi.org/10.1016/j.pccm.2026.05.001View
Published (Version of record) Open Access

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.
Stem Cells Mucus hypersecretion Mucus plugging Obstructive lung disease Submucosal glands

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