role of camkii and pka in early afterdepolarization of human ventricular myocardium cell: a computational model study
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2016
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Abstract
Early afterdepolarization (EAD) plays an important role in arrhythmogenesis. Many experimental studies have reported that Ca2+/calmodulin-dependent protein kinase II (CaMKII) and β-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 β-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 (INaL) deactivation progress; (2) the combined effect of CaMKII overexpression and activation of β-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 (IKr) blockage (77% versus 85%). In summary, this study computationally demonstrated the combined role of CaMKII and β-adrenergic signaling pathway on the occurrence of EADs, which could be useful for searching for therapy strategies to treat EADs related arrhythmogenesis.
| Reference Key |
dai2016computationalrole
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|---|---|
| Authors | ;Ling Dai;Yunliang Zang;Dingchang Zheng;Ling Xia;Yinglan Gong |
| Journal | advanced functional materials |
| Year | 2016 |
| DOI |
10.1155/2016/4576313
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| URL | |
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