Treatment with senicapoc, a KCa3.1 channel blocker, alleviates hypoxemia in a mouse model for acute respiratory distress syndrome.

Asbjørn Graver PetersenPeter Carøe LindSusie MogensenAnne-Sophie Bonde JensenAsger GranfeldtUlf Simonsen

Published in: British journal of pharmacology (2021)

Genetic deficiency of KCa3.1 channels and senicapoc improved the PaO2 /FiO2 ratio and decreased the cytokines after a ventilator-induced lung injury. Moreover, senicapoc directly affects lung epithelial cells and blocks neutrophil infiltration of the injured lung. These findings open the perspective that blocking KCa3.1 channels is a potential treatment in ARDS-like disease.

Keyphrases

acute respiratory distress syndrome
extracorporeal membrane oxygenation
mechanical ventilation
mouse model
oxidative stress
replacement therapy
combination therapy
climate change
risk assessment
genome wide
copy number
endothelial cells
human health
angiotensin converting enzyme