Activation of the NLRP3-inflammasome/CaMKII pathway in atrial cardiomyocytes provides a molecular substrate for postoperative atrial fibrillation.
Preexisting Ca2+-handling abnormalities and activation of NLRP3-inflammasome/CaMKII signaling are evident in atrial cardiomyocytes from patients who subsequently develop POAF. These molecular substrates sensitize cardiomyocytes to spontaneous Ca2+-releases and arrhythmogenic afterdepolarizations, particularly upon exposure to inflammatory mediators. Our data reveal a potential cellular and molecular substrate for this important clinical problem.
Heijman et al. (2020) studied this question.