Regulatory mechanism of calcium/calmodulin-dependent protein kinase II in the occurrence and development of ventricular arrhythmia (Review)

Ventricular arrhythmia (VA) is a highly fatal arrhythmia that involves multiple ion channels. Of all sudden cardiac death events, similar to 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.

Automated summary

Ventricular arrhythmia (VA) is a highly fatal arrhythmia involving multiple ion channels, and activated CaMKII plays a key role in this condition by regulating ion channels in the heart. Understanding the mechanisms of VA based on the CaMKII pathway is crucial for clinical treatment and drug development.