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• W2090925419 endingPage "132" @default.
• W2090925419 startingPage "117" @default.
• W2090925419 abstract "<b><i>Background:</i></b> In cystic fibrosis (CF), genetic mutations in the CF transmembrane conductance regulator (CFTR) gene cause reduced chloride efflux from ciliated airway epithelial cells. This results in a reduction in periciliary liquid (PCL) depth of the airway surface liquid due to associated reduced water efflux. PCL layer dehydration reduces mucociliary clearance (MCC), leading to airway obstruction (reduced airflow and inflammation due to pathogen invasion) with mucus plug formation. <b><i>Summary:</i></b> Rehydrating mucus increases MCC. Mucus hydration can be achieved by direct hydration (administering osmotic agents to set up an osmotic gradient), using CFTR modulators to correct dysfunctional CFTR, or it can be achieved pharmacologically (targeting other ion channels on airway epithelial cells). <b><i>Key Messages:</i></b> The molecular mechanisms of several therapies are discussed in the context of pre-clinical and clinical trial studies. Currently, only the osmotic agent 7% hypertonic saline and the CFTR ‘potentiator' VX-770 (ivacaftor) are used clinically to hydrate mucus. Emerging therapies include the osmotic agent mannitol (Bronchitol), the intracellular Ca²⁺-raising agent Moli1901/lancovutide, the CFTR potentiator sildenafil [phosphodiesterase type 5 (PDE5) inhibitor] and the CFTR ‘corrector' VX-809 (lumacaftor). Other CFTR correctors (e.g. ‘chemical chaperones') are also showing pre-clinical promise." @default.
• W2090925419 created "2016-06-24" @default.
• W2090925419 creator A5005714301 @default.
• W2090925419 creator A5067582404 @default.
• W2090925419 date "2015-01-01" @default.
• W2090925419 modified "2023-09-27" @default.
• W2090925419 title "Therapeutic Options for Hydrating Airway Mucus in Cystic Fibrosis" @default.
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