Table 1.

CaMKII in AF: summary of animal studies

Author	Year	Species	Arrhythmia model	CaMKII	Effect
Greiser et al.88	2009	Goat	Rapid atrial pacing	CaMKII-dependent hyperphosphorylation of RyR2	Atrial hypocontractility Decreased SR Ca2+ load
Chelu et al.89	2009	Mouse	Genetic mouse model (CREM-IbΔC-X transgenic mice)	Increased expression and autophosphorylation of CaMKIIδ	Hyperphosphorylation of RyR2, arrhythmia suppression by CaMKII inhibition.
Chelu et al.89	2009	Goat	Rapid atrial pacing	Increased expression and autophosphorylation of CaMKIIδ	Hyperphosphorylation of RyR2
Wakili et al.90	2010	Canine	Rapid atrial pacing	Increased expression and autophosphorylation of CaMKIIδ	Atrial hypocontractility Decreased APD Decreased Ca2+ transient
Purohit et al.66	2013	Mouse	Angiotensin-II	Increased ox-CaMKII	Increased AF susceptibility dependent on ox-CaMKIIδ and RyR2 S2814 phosphorylation, arrhythmia suppression by CaMKII inhibition
Greiser et al.91	2014	Rabbit	Atrial myocytes	No change in CaMKII-dependent RyR2 phosphorylation or CaMKII activity	Ca2+ signalling silencing with increased intracellular Ca2+ and no changes in Ca2+ sparks, Ca2+ waves, Ca2+ release, and Ca2+ release instability
Fischer et al.56	2015	Mouse	Atrial cardiomyocytes treated with ATX-II	Increased p-CaMKII	Enhanced late INa Increased SR Ca2+-leak Hyperphosphorylation of CaMKII target sites: RyR2 (Ser2815) and PLN (Thr17)
Lenski et al.92	2015	NVRM	Electrical stimulation	Increased p-CaMKII/CaMKII	Increased p-AMPK/AMPK Increased FA uptake Decreased glucose uptake

AP, action potential; AMPK, AMP-activated protein kinase; ATX-II, Anemonia-sulcata toxin-II; FA, fatty acid; NVRM, neonatal ventricular rat myocytes; ox-CaMKII, oxidized CaMKII; p-CaMKII, phosphorylated CaMKII; p-AMPK, phosphorylated AMPK; PLN, phospholamban; SR, sarcoplasmic reticulum; RyR2, ryanodine type 2 receptor.