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    One therapeutic strategy for cystic fibrosis (CF) seeks to restore anion transport to affected epithelia by targeting other apical membrane Cl- channels to bypass dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel. The properties and regulation of the Ca2+-activated Cl- channel TMEM16A argue that long-acting small molecules which target directly TMEM16A are required to overcome CFTR loss. Through genetic studies of lung diseases, SLC26A9, a member of the solute carrier 26 family of anion transporters, has emerged as a promising target to bypass CFTR dysfunction. An alternative strategy to circumvent CFTR dysfunction is to deliver to CF epithelia artificial anion transporters that shuttle Cl- across the apical membrane. Recently, powerful, non-toxic, biologically-active artificial anion transporters have emerged. Copyright © 2017. Published by Elsevier Ltd.


    Hongyu Li, Johanna J Salomon, David N Sheppard, Marcus A Mall, Luis Jv Galietta. Bypassing CFTR dysfunction in cystic fibrosis with alternative pathways for anion transport. Current opinion in pharmacology. 2017 Oct 21;34:91-97

    PMID: 29065356

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