Emerging molecular therapies targeting myocardial infarction-related arrhythmias: the role of miRNAs regulation

We read the article by Driessen et al.¹ with great interest, and congratulate the authors on their excellent work. As the authors correctly state, an approach to speed conduction and prevent re-entry-based arrhythmias in myocardial infarction (MI) may stem from interference with the micro-RNA, miR1.¹ However, we would like to point out two important aspects. First, there is evidence that miR-1231 is overexpressed after MI insults while calcium channel voltage-dependent alpha 2/delta subunit 2 (Cacna2d2) (identified as the target of miR-1231) is suppressed by miR-1231 and that the forced overexpression of miR-1231 promotes arrhythmias while the inhibition of miR-1231 ameliorates arrhythmias in ischaemic hearts. Thus, these results shed light on the important arrhythmogenic function of miR-1231 in MI and suggest that its inhibition may serve as a potential antiarrhythmic ischaemic therapy.² Second, there is also evidence that upregulation of miR-223-3p in MI represses the expression of KCND2/Kv4.2 resulting in reduction of Ito density that can cause action potential duration (APD) prolongation and can promote arrhythmias in MI. Therefore also knockdown of endogenous miR-223-3p might be considered a new approach for antiarrhythmic ischaemic therapy.^3,4 The findings of Driessen et al.¹ add significant informations to previously published data and they correctly highlight the role of miR1 interference but evaluating the real effect of the role of other miRNAs regulation as specific treatment strategies would be useful for better improving myocardial infarction-related arrhythmias.

Acknowledgments

Salvatore Patanè wrote the letter, Francesco Patanè prepared the references.

Conflict of interest: none declared.

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