Enhanced cardiomyocyte reactive oxygen species signaling promotes ibrutinib-induced atrial fibrillation

In conclusion, our study has established a pathophysiological role for ROS signaling in atrial cardiomyocytes, and it may be that ox-CaMKII and p-CaMKII (Thr-286) are activated by ROS to increase AF susceptibility following ibrutinib treatment. We have also identified the inhibition of NOX as a potential novel AF therapy approach.
Source: Redox Biology - Category: Biology Source Type: research