Inhibition of the K(Ca)3.1 Channel Alleviates Established Pulmonary Fibrosis in a Large Animal Model
Louise Organ, Barbara Bacci, Emmanuel Koumoundouros, Wayne G Kimpton, Chrishan S Samuel, Cameron J Nowell, Peter Bradding, Katy M Roach, Glen Westall, Jade Jaffar, Ken J Snibson
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY | AMER THORACIC SOC | Published : 2017
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive disease of increasing prevalence marked by poor prognosis and limited treatment options. Ca2+-activated KCa3.1 potassium channels have been shown to play a key role in the aberrant activation and responses to injury in both epithelial cells and fibroblasts, both considered key drivers in the fibrotic process of IPF. Pharmacological inhibition of IPF-derived fibroblasts is able to somewhat prevent TGF-β- and basic fibroblast growth factor-dependent profibrotic responses. In the current study, we investigated whether blockade of the KCa3.1 ion channel in vivo with a selective inhibitor, Senicapoc, was able to attenuate both histolog..View full abstract
Awarded by National Health and Medical Research Council Australia Senior Research Fellowship
This work was supported by National Health and Medical Research Council Australia Senior Research Fellowship GNT1041766 (C.S.S.).