Mitra Mithun, Coller Hilary A
Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, CA, USA;; Department of Biological Chemistry, David Geffen School of Medicine, Los Angeles, CA, USA.
Ann Transl Med. 2016 Dec;4(23):469. doi: 10.21037/atm.2016.11.39.
An increase in stress-associated microRNAs has been observed in the heart after an induced myocardial infarction. Liu and colleagues now demonstrate that one of these stress-associated microRNAs, , can regulate a component of the voltage-gated channel that mediates rapid outward efflux of potassium during an action potential. Aberrations in the potassium current have been associated with ventricular arrhythmia and heart disease. Strikingly, introducing a small RNA antagonist directed against into rat hearts, while also inducing a myocardial infarction, resulted in a reduction in arrhythmias. We place these studies in the larger context of the field and discuss the potential of anti- molecules as new therapeutics for myocardial infarction.
在诱导性心肌梗死后的心脏中,已观察到与应激相关的微小RNA增加。刘及其同事现在证明,这些与应激相关的微小RNA之一,可以调节电压门控通道的一个组成部分,该通道在动作电位期间介导钾的快速外向流出。钾电流异常与室性心律失常和心脏病有关。令人惊讶的是,将针对该微小RNA的小RNA拮抗剂引入大鼠心脏,同时诱导心肌梗死,可导致心律失常减少。我们将这些研究置于该领域的更大背景下,并讨论抗微小RNA分子作为心肌梗死新疗法的潜力。