These could include atrial-selective ion channels (e.g. atrial I(Na), I(Kur) and I(K,ACh)), pathology-selective ion channels (constitutively active I(K,ACh), TRP channels), ischemia-uncoupled gap junctions, proteins related to malfunctioning intracellular Ca2+ homeostasis (e.g., "leaky" ryanodine receptors, overactive Na+, Ca2+ exchanger) or risk factors for arrhythmias ("upstream" therapies).
Our data demonstrate that the n-3 PUFAs significantly suppress cardiac I(NCX1), which is probably one of their protective effects against lethal arrhythmias.