自噬作为细胞自我保护机制，在心肌缺血再灌注损伤(IRI)中却发挥“双刃剑”效应。在总结前人与自身工作基础上，我们假设lncRNA-4321/miR-702-5p/Notch1轴向调控自噬，减轻心肌IRI。在多参数确认自噬性心肌保护作用前提下，从细胞活力、心梗面积、左心功能等经典指标，在体内外水平阐明Notch1通过增强自噬，减轻心肌IRI；利用转基因介导的回补实验，探讨miR-702-5p下调Notch1表达，削弱自噬性心肌保护作用；应用双荧光素酶报告基因与biotin-avidin pulldown技术研究lncRNA-4321以miR-702-5p为节点调控Notch1表达的分子机理，再分层论述lncRNA-4321/miR-702-5p/Notch1轴向调控自噬，减轻心肌IRI的生物效应，旨在揭示lncRNA/miRNA防治心肌IRI的分子机制，为临床心肌保护策略提供新的理论依据。

Despite appreciated as a cellular self-protection mechanism, autophagy functions as a double-edged sword on myocardial ischemia reperfusion injury(IRI). Based on previous publications and our preliminary data, we hypothesize that lncRNA-4321/miR-702-5p/Notch1 axial reduces myocardial IRI through regulation of autophagy. On the premise of clarifying the cardioprotective effect of autophagy, we will elucidate the biological effects of Notch1 on reducing myocardial IRI by enhancing autophagy in series experiments in vitro and in vivo, such as cell viability, infarct size and left heart function. Transgenic mediated compensation experiment will be utilized to demonstrate that miR-702-5p reduces the cardioprotective effect of autophagy by downregulation of Notch1 expression. Dual luciferase reporter gene assay and biotin-avidin pulldown experiments will be applied to investigate the molecular mechanism of lncRNA-4321 in regulating the expression of Notch1 depend on miR-702-5p, transgenic technology will be employed to investigate the physiological function of lncRNA-4321/miR-702-5p/Notch1 axial in reducing myocardial IRI through regulation of autophagy. In short, this study will reveal the molecular mechanism of lncRNA/miRNA in heart protection against myocardial IRI, and will provide a novel strategy for clinical myocardial protection.