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首页> 外文期刊>Journal of cardiovascular translational research. >Inhibition of MicroRNA-206 Ameliorates Ischemia-Reperfusion Arrhythmia in a Mouse Model by Targeting Connexin43
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Inhibition of MicroRNA-206 Ameliorates Ischemia-Reperfusion Arrhythmia in a Mouse Model by Targeting Connexin43

机译:抑制 MicroRNA-206 通过靶向连接蛋白 43 改善小鼠模型中的缺血再灌注心律失常

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摘要

Reperfusion arrhythmias (RA) are an important cause of sudden cardiac death and is closely associated with gap junction protein in the heart, connexin 43 (Cx43). This study is aimed at elucidating the molecular association between microRNA-206 (miR-206) and Cx43 in ischemia-reperfusion arrhythmia using experimental animal model. Our results showed that miR-206 inhibitor alleviated ischemia-reperfusion-induced arrhythmias, indicated by the lower extent of changes in heart rate (HR), PR interval, rate pressure product (RPP), and mean arterial pressure (MAP). miR-206 inhibitor also downregulated the serum creatine kinase isoenzyme (CKMB) and cardiac troponin I (cTnI) levels in mice under myocardial ischemia-reperfusion (IR) process. The knockdown of Cx43 inversed the protective effects of miR-206 inhibitor on cardiac arrhythmias. These results supported that inhibition of miR-206 ameliorates ischemia-reperfusion arrhythmia by targeting Cx43, and this miR-206/Cx43 axis could serve as a potential target for the management of ischemic-perfusion arrhythmia.
机译:再灌注心律失常 (RA) 是心源性猝死的重要原因,与心脏中的间隙连接蛋白连接蛋白 43 (Cx43) 密切相关。本研究旨在利用实验动物模型阐明缺血再灌注心律失常中microRNA-206(miR-206)与Cx43的分子关联。我们的结果表明,miR-206抑制剂缓解了缺血再灌注引起的心律失常,表现为心率(HR)、PR间期、心率压力积(RPP)和平均动脉压(MAP)的变化程度较低。miR-206抑制剂在心肌缺血再灌注(IR)过程中也下调小鼠血清肌酸激酶同工酶(CKMB)和心肌肌钙蛋白I(cTnI)水平。Cx43的敲除逆转了miR-206抑制剂对心律失常的保护作用。这些结果支持抑制 miR-206 通过靶向 Cx43 改善缺血再灌注性心律失常,并且该 miR-206/Cx43 轴可作为缺血性灌注性心律失常治疗的潜在靶点。

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