Figure 3.

CaMKII transduces proarrhythmic signalling in atrial remodelling and AF in a feed-forward manner. Increased intracellular Ca²⁺ and ROS induce autonomous CaMKII activity. Excessive CaMKII activity through its action on multiple downstream targets (ion channels, proteins, etc.) results in triggered and reentrant activities that can initiate and perpetuate AF. It also results in several changes that are associated with atrial remodelling in AF. Underlying disease states or risk factors also cause excessive CaMKII activity with similar proarrhythmic downstream consequences. HF, heart failure; SND, sinus node dysfunction.