缺血性心律失常（尤室颤、室速）是心肌梗死发生猝死的主要因素，机制尚不明确，也缺乏有效的防治措施。我们前期研究发现，Apelin作为新型心血管保护因子，其血清水平与心肌梗死患者发生缺血性心律失常具有显著的相关性，但其对缺血性心律失常的作用尚无报道。本项目通过动物模型、细胞培养及转基因动物，应用分子生物学、膜片钳等技术，研究Apelin对缺血时心肌钠、钾和钙离子通道的作用及下游信号通路，探讨其对缺血性心律失常的调控机制，寻找并构建缺血时lncRNAs- MicroRNAs-Apelin的分子调控网络，证实通路MIAT-miR-503/15b-Apelin-离子通道参与缺血性心律失常的发生，并结合心肌梗死患者血液样品的数据分析，寻找缺血性心律失常相关的预警生物标志物。本项目将完善并拓展我们对缺血性心律失常发病机制和防治策略的认识，为缺血性心律失常的新药研发提供理论依据和治疗靶点。

Ischemic arrhythmias such as ventricular tachycardia and ventricular fibrillation were the most common reasons of sudden cardiac death. But its mechanism was not clear and in clinic there were lack of effective prevention measures for ischemic arrhythmias. In our preliminary study, we found that Apelin, as one of the new protective factors on cardiovascular system, was negative correlated with the occurrences of ischemic arrhythmias in myocardio infarction (MI), therefore we speculated that Apelin is an important regulator associated with ischemic arrhythmias in MI, but the detailed mechanisms have not been elucidated. This project will use the Apelin knockout mice, Patch-clamp and molecular biological techniques, etc. to determine if Apelin is involved in ionic remodeling such as sodium, calcium and potassium channels, to clarify the molecular mechanisms and identify that Apelin will be a therapeutic target for ischemic arrhythmias. To find and build the molecula network of lncRNAs-MicroRNAs-Apelin in MI. To confirm that the signal pathway MIAT-miR-503/15b-Apelin-ion channels was involved in the ischemic arrhythmias. To collect the serum samples of patients with MI and search the related warning biomarkers for ischemic arrhythmias .The project will provide new insights into the treatment of ischemic arrhythmias and the prevention of sudden cardiac death.