Activation of the NLRP3-inflammasome/CaMKII pathway in atrial cardiomyocytes provides a molecular substrate for postoperative atrial fibrillation.
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NLRP3-inflammasome/CaMKII activation may promote postoperative AF susceptibility; leaves open targeted inhibition in patients.
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.
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Heijman et al. (2020) studied this question.
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