Early afterdepolarization (EAD) plays an important role in arrhythmogenesis. Many experimental studies have reported that Ca/calmodulin-dependent protein kinase II (CaMKII) and -adrenergic signaling pathway are two important regulators. In this study, we developed a modified computational model of human ventricular myocyte to investigate the combined role of CaMKII and -adrenergic signaling pathway on the occurrence of EADs. Our simulation results showed that (1) CaMKII overexpression facilitates EADs through the prolongation of late sodium current's () deactivation progress; (2) the combined effect of CaMKII overexpression and activation of -adrenergic signaling pathway further increases the risk of EADs, where EADs could occur at shorter cycle length (2000 ms versus 4000 ms) and lower rapid delayed rectifier K current () blockage (77% versus 85%). In summary, this study computationally demonstrated the combined role of CaMKII and -adrenergic signaling pathway on the occurrence of EADs, which could be useful for searching for therapy strategies to treat EADs related arrhythmogenesis.
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| http://dx.doi.org/10.1155/2016/4576313 | DOI Listing |
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