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Phlegm removal is a physiological process, not a molecular target. It involves the elimination of thickened mucus (phlegm) from the airways, mainly through mucociliary transport and the act of coughing[1][3][4][6][7]. The process is critical for defending the respiratory system against pathogens, pollutants, and allergens, and relies on the coordinated action of cilia, mucus properties (produced by goblet cells and submucosal glands), and fluid secretion mechanisms. In disease states such as cystic fibrosis and COPD, phlegm removal is impaired, requiring pharmacological (mucolytics, expectorants) and/or mechanical (chest physiotherapy) support[2][5][7]. Drug targets for interventions tend to focus on ion channels (e.g., CFTR, ENaC), purinergic receptors (e.g., P2Y~2~), and other modulators, but "phlegm removal" itself is not a molecule or receptor. This entry should be mapped to relevant molecular targets such as "Mucin proteins", "Cystic fibrosis transmembrane conductance regulator (CFTR)", or "P2Y~2~ receptor" for structured biomedical databases[2][4][6].
Reduction of mucus viscosity; Stimulation of ciliary activity; Hydration of airway surface; Mechanical clearance by coughing
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