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Ion channel messenger RNA processing defects and arrhythmia

Authors Zhou A, Dudley Jr S

Received 24 August 2014

Accepted for publication 16 October 2014

Published 24 November 2014 Volume 2014:4 Pages 151—160


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Hung Khong

Anyu Zhou, Samuel C Dudley Jr

Lifespan Cardiovascular Research Center, The Warren Alpert School of Medicine, Brown University, and Providence Veterans Administration Medical Center, Providence, RI, USA

Abstract: Messenger RNA (mRNA) processing is an essential step for the expression of most eukaryote genes. Ion channels are critical for proper electrical activity in the heart, and perturbations of these channels are known to cause arrhythmia. Recently, mRNA processing defects have been shown to contribute to altered ion channel activity and arrhythmogenesis. Abnormal pre-mRNA splicing of cardiac ion channels, including the cardiac sodium channel, potassium channels, and calcium channels, because of mutations of the cis-elements within the RNA or abnormal expression of splicing factors, has been documented to contribute to arrhythmic risk. In addition to pre-mRNA splicing, other mRNA processing events, such as 3'-end formation and mRNA turnover, are also disrupted in cardiac diseases, such as congenital heart disease caused by mutation at the 3'-untranslated region of GATA4. mRNA stability is also dysregulated by altered expression of microRNAs in atrial fibrillation. In this review, we discuss our current understanding of how mRNA processing defects contribute to the risk of arrhythmias and how monitoring the products of abnormal processing may lead to diagnostic tests for arrhythmic risk.

Keywords: messenger RNA, arrhythmia, sudden death, ion channels, biomarkers

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