Figure. Schematic outlines triggered arrhythmic activities through the relevant mechanisms of coupled kinases and ion channels.

Physiological and pathological regulation of ca²⁺ dynamics occur in myocytes through a number of kinases including the CaMKII (Ca²⁺/calmodulin-kinase type-II), PKA (protein kinase A), JNK (c-Jun N-terminal kinase) signaling pathways. Sleep disordered breathing (SDB) facilitates proarrhythmic activities and atrial fibrillation through a CaMKII-dependent dysregulation of I_Na,L and sarcoplasmic reticulum (SR) Ca²⁺ mishandling. SDB may act as a cellular stressor manifesting its affects via hypoxia-ischemic input which could involve the PKA and JNK pathways or other yet to be identified pathways. β-AR indicates β-adrenergic receptor; AC, adenylyl cyclase; c-AMP, cyclic adenine monophosphate; CaM, calmodulin; DAD, delayed afterdepolarization; EAD, early afterdepolarization; I_Na,L, late Na channel; I_Ca, Ca²⁺ current; NCX, Na⁺/Ca²⁺ exchanger; PLB, phospholipase B; and ROS, reactive oxygen species.