Bypassing CFTR dysfunction in cystic fibrosis with alternative pathways for anion transport

Hongyu Li, Johanna J Salomon, David N Sheppard, Marcus A Mall, Luis Jv Galietta

Research output: Contribution to journalArticle (Academic Journal)peer-review

55 Citations (Scopus)
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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 Ca(2+)-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.

Original languageEnglish
Pages (from-to)91-97
Number of pages7
JournalCurrent Opinion in Pharmacology
Early online date21 Oct 2017
Publication statusPublished - 2017

Bibliographical note

Issue cover date: June 2017


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