The role of microRNA in cardiac excitability.
Cardiomyocytes are excitable cells that can generate and propagate excitations; excitability is a fundamental characteristic of these cells, which is reflected by action potential; the changes of transmembrane potential as a function of time; and orchestrated by ion channels, transporters, and cellular proteins. The electrical excitation evoked in muscles must be transformed into mechanical contraction through the so-called excitation-contraction coupling mechanism, and the proper contraction of cardiac muscles then drives pumping of blood to the body circulation. Arrhythmias are electrical disturbances that can result in irregular heart beating with consequent insufficient pumping of blood. Arrhythmias are often lethal, constituting a major cause for cardiac death, particularly sudden cardiac death, in myocardial infarction and heart failure. Recent studies have led to discovery of microRNAs (miRNAs) as a new player in the cardiac excitability by fine-tuning expression of ion channels, transporters, and cellular proteins, which determines the arrhythmogenicity in many conditions. This review article will give a comprehensive summary on the data available in the literature. The basics of cardiac excitability will first be introduced, followed by a brief introduction to the basics of miRNAs. Then, studies on regulation of cardiac excitability by miRNAs will be described and analyzed. Finally, concluding remarks will be provided.
Wang
Zhiguo
Z
Research Center, Montreal Heart Institute, Department of Medicine, University of Montreal, Montreal, Canada. zhiguo.wang@icm-mhi.org
D000200:Action Potentials; D001145:Arrhythmias, Cardiac / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D005786:Gene Expression Regulation; D006329:Heart Conduction System / Q000502:physiology; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007473:Ion Channels / Q000235:genetics / Q000502:physiology; D035683:MicroRNAs / Q000502:physiology*; D009203:Myocardial Infarction / Q000378:metabolism / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000502:physiology
D007473:Ion Channels; D035683:MicroRNAs