心肌缺血再灌注损伤是影响冠心病再灌注疗效的重要因素。既往及前期研究发现，凋亡、自噬和程序性坏死介导的心肌细胞程序性死亡，是心肌缺血再灌注损伤的关键节点。cFLIP作为重要的转录因子，通过调节多个效应基因，可能参与调控这一病理过程。本课题拟通过：(1)检测上调cFLIPS和（或）cFLIPL对缺氧/复氧诱导的心肌细胞死亡的影响及内在机制，探讨cFLIP介导的程序性细胞死亡是否具有“有效”和“多效”保护心肌细胞的作用；(2)构建大鼠心肌缺血再灌注损伤模型，检测上调cFLIPS和（或）cFLIPL对心肌梗死面积和心功能的影响，探讨cFLIP介导的程序性细胞死亡对心肌缺血再灌注损伤的作用。通过本项目的实施，可进一步阐明心肌缺血再灌注损伤的发病机制，为冠心病再灌注损伤的防治提供新的治疗策略。

Myocardial ischemia-reperfusion injury plays an important role in reperfusion therapy of coronary artery disease. Previous and our studies have found myocardial programmed cell death including apoptosis, autophagy and necrosis, is a key node of myocardial ischemia-reperfusion injury. cFLIP, as an important transcription factor, regulating multiple effect genes, may participate in this pathological process. In present study, we attempt to (1) detect the effect and potential mechanism of cFLIPS and (or) cFLIPL over-expression on myocardial cell death induced by hypoxia/reoxygenation, in order to explore the efficiency and pleiotropy of programmed cell death mediated by cFLIP on myocardial protection; (2)build ischemia-reperfusion injury rat model, and evaluate effects of cFLIPS and (or) cFLIPL over-expression on myocardial infarction area and cardiac function, so as to reveal the role of programmed cell death mediated by cFLIP in myocardial ischemia-reperfusion injury. On the basis of successful application of our study, the pathogenesis of myocardial ischemia-reperfusion injury can be further elucidated, and a new therapeutic strategy of coronary artery disease reperfusion will be provided.