Abstract
MicroRNA-26 (miR-26) is predicted to target the gene encoding KIR2.1, KCNJ2. Luo et al (J Clin Invest 2013; 123:1939, PMID 23543060) found that miR-26 was downregulated in atrial samples from atrial fibrillation (AF) animals and patients and this downregulation was accompanied by the upregulation of the IK1/KIR2.1 protein. The overexpression of miR-26 suppressed the expression of KCNJ2/KIR2.1. In contrast, miR-26 knockdown, inhibition, or binding-site mutation enhanced KCNJ2/KIR2.1 expression, establishing KCNJ2 as a miR-26 target. The knockdown of endogenous miR-26 promoted AF in mice, whereas adenovirus-mediated expression of miR-26 reduced AF vulnerability. The authors conclude that miR-26 controls the expression of KCNJ2 and suggest that this downregulation may promote AF.
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