急性心肌缺血导致细胞线粒体凋亡一直是冠心病研究重点关注的问题。前期研究发现：（1）急性心肌梗死患者外周血中lncRNA-MALAT1高表达；（2）lncRNA-MALAT1与miR-205存在结合位点；（3）lncRNA-MALAT1调控肿瘤细胞凋亡。据此推测lncRNA-MALAT1/miR-205/Akt轴向调控急性心肌缺血细胞线粒体凋亡，但具体机制不明确。本项目采用缺血缺氧细胞和动物模型，靶向沉默lncRNA-MALAT1，通过miR-205 mimic、Akt阻断剂干预及RIP等技术，揭示lncRNA-MALAT1/miR-205/Akt轴向关系，阐明沉默lncRNA-MALAT1介导miR-205/Akt减少细胞线粒体凋亡的分子机制，探究lncRNA-MALAT1调控细胞线粒体凋亡关键因子和作用机制。并进行临床验证，为急性心肌缺血的靶向干预和预后评价提供新的思路。

Mitochondrial apoptosis induced by acute myocardial ischemia is always the emphasis in the research of coronary artery disease. Our previous studies have found: (1) lncRNA-MALAT1 was high expression in peripheral blood of acute myocardial infarction patient, (2) lncRNA-MALAT1 bound with miR-205, (3) lncRNA-MALAT1 regulated tumor cells apoptosis. It was presumed that lncRNA-MALAT1/miR-205/Akt would regulate the mitochondrial apoptosis during acute myocardial ischemia， but the mechanisms are not clear. The project will establish the hypoxia ischemia model of cell and animal to study the relationship among lncRNA-MALAT1/ miR-205/Akt and explore the mechanism of lncRNA-MALAT1 regulating miR-205/Akt in mitochondria apoptosis by lncRNA-MALAT1 silencing, miR-205 mimic, Akt specific inhibitor intervention and RNA banding protein precipitation (RIP). The project will also use clinical verifications to provide a new idea for targeted intervention and prognostic evaluation of acute myocardial ischemia.