Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma

Abstract

features of allergic asthma were regulated in part by Mt-CaMKII-mediated, Mt-ROS-induced activation of NF-B and the NLRP3 inflammasome. Taken together, our findings suggest that airway epithelial cellderived Mt-CaMKII increases Mt-ROS that promotes induction of core features of allergic asthma. These data implicate Mt-CaMKII in multiple processes in the development of asthma. Mitochondrial-localized CaMKII inhibition may provide a new potential candidate target for future asthma therapies.