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 SimonsenPublished 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.