Mucin (MUC5AC and MUC5B) (MUC)

Mucins are high-molecular-weight glycoproteins that constitute the primary structural framework of the mucus gel layer, which protects and lubricates epithelial surfaces [1]. In the human airway, the gel-forming mucins MUC5AC and MUC5B are the most prominent, playing a vital role in the innate immune system by trapping inhaled particles and pathogens for removal via mucociliary clearance [1, 2]. Pathological conditions such as asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis are characterized by mucus hypersecretion, where excessive mucin expression and secretion lead to airway plugging, reduced lung function, and increased infection risk [1, 5]. Therapeutic strategies focus on reducing the burden of mucus by either breaking down the physical structure of secreted mucins (mucolytics), inhibiting the signaling pathways (such as EGFR or IL-13/STAT6) that drive mucin gene expression, or blocking the intracellular mechanisms (like the MARCKS protein) responsible for the rapid exocytosis of mucin granules [3, 4]. Effective modulation of mucin dynamics is essential for alleviating symptoms and preventing disease progression in patients with chronic obstructive airway diseases [5].

Other names

Mucus hypersecretionMucin productionAirway mucusMucin synthesis

Therapeutic modulation involves three main approaches: mucolytics (e.g., N-acetylcysteine) break disulfide bonds to reduce mucus viscosity [4]; anti-inflammatory agents and biologics (e.g., corticosteroids, Dupilumab) inhibit signaling pathways like IL-13/STAT6 or EGFR to suppress mucin gene expression [1, 5]; and MARCKS protein inhibitors (e.g., BIO-11006) block the intracellular transport and exocytosis of mucin granules from goblet cells [3].