Abstract
Correction of CF lung abnormalities may be obtained by restoring the function of CFTR with mutation-specific treatments. A potentially alternative approach is to modulate the activity of other targets to stimulate CFTR-independent anion secretion or inhibit acidification. Despite the increasing interest towards possible alternative targets such as TMEM16A, SLC26A9, SLC26A4 and ATP12A, their precise function and expression in the airways is largely unknown or controversial, and specific modulators are still lacking.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
