Regulatory mechanism of calcium/calmodulin‑dependent protein kinase II in the occurrence and development of ventricular arrhythmia (Review)
- Kexin Ma
- Guoping Ma
- Zijing Guo
- Gang Liu
- Wenjie Liang
Affiliations: Graduate School, Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China, College of Integrated Traditional Chinese and Western Medicine, Hebei University of Chinese Medicine, Shijiazhuang, Hebei 050200, P.R. China
- Published online on: April 20, 2021 https://doi.org/10.3892/etm.2021.10088
Copyright: © Ma
et al. This is an open access article distributed under the
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Ventricular arrhythmia (VA) is a highly fatal arrhythmia that involves multiple ion channels. Of all sudden cardiac death events, ~85% result from VAs, including ventricular tachycardia and ventricular fibrillation. Calcium/calmodulin‑dependent pro‑tein kinase II (CaMKII) is an important ion channel regulator that participates in the excitation‑contraction coupling of the heart, and as such is important for regulating its electrophysiological function. CaMKII can be activated in a Ca2+/calmodulin (CaM)‑dependent or Ca2+/CaM‑independent manner, serving a key role in the occurrence and development of VA. The present review aimed to determine whether activated CaMKII induces early afterdepolarizations and delayed afterdepolarizations that result in VA by regulating sodium, potassium and calcium ions. Assessing VA mechanisms based on the CaMKII pathway is of great significance to the clinical treatment of VA and the de‑velopment of effective drugs for use in clinical practice.