Pacemaker activity and ion channels in the sinoatrial node cells: MicroRNAs and arrhythmia

The primary pacemaking activity of the heart is determined by a spontaneous action potential (AP) within sinoatrial node (SAN) cells. This unique AP generation relies on two mechanisms: membrane clocks and calcium clocks. Nonhomologous arrhythmias are caused by several functional and structural changes in the myocardium. MicroRNAs (miRNAs) are essential regulators of gene expression in cardiomyocytes. These miRNAs play a vital role in regulating the stability of cardiac conduction and in the remodeling process that leads to arrhythmias. Although it remains unclear how miRNAs regulate the expression and function of ion channels in the heart, these regulatory mechanisms may support the development of emerging therapies. This study discusses the spread and generation of AP in the SAN as well as the regulation of miRNAs and individual ion channels. Arrhythmogenicity studies on ion channels will provide a research basis for miRNA modulation as a new therapeutic target.

Automated summary

The pacemaking activity of the heart is primarily determined by spontaneous action potentials (APs) within sinoatrial node (SAN) cells, which rely on membrane clocks and calcium clocks. Nonhomologous arrhythmias result from changes in myocardial function and structure. MicroRNAs (miRNAs) are important regulators of gene expression in cardiomyocytes and play a role in regulating cardiac conduction stability and arrhythmia-induced remodeling. Although the mechanisms of miRNA regulation of ion channels in the heart are not yet clear, these mechanisms may support new therapeutic approaches. This study discusses AP generation and spread in the SAN, as well as the regulation of miRNAs and individual ion channels, with the aim of providing a research basis for miRNA modulation as a new therapeutic target for arrhythmias.