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细胞焦亡是一种新发现的细胞程序性死亡方式，该过程包含多种细胞因子的激活与降解。首先，细胞内炎症小体被激活，进而诱导半胱天冬酶（caspase）-1的激活和促炎症因子IL-1 和IL-18前体的降解。之后，细胞膜裂解与细胞核DNA片段化可导致IL-1 和IL-18释放，最终诱发炎症反应。机体固有免疫细胞经模式识别受体，识别病原相关分子模式或损伤相关分子模式，诱发细胞焦亡而清除病原体或损伤组织细胞，形成保护机体的一道有效屏障。越来越多的研究表明，在动脉粥样硬化(AS)的病理过程中，细胞焦亡不仅参与动脉粥样斑块的形成，也是促进斑块发展，甚至是影响斑块稳定性的重要因素。在心肌缺血/再灌注损伤中，细胞焦亡亦是MI区与边界区炎症反应的重要调控因子，其可影响修复期MI面积、纤维化程度与心功能。因此，细胞焦亡可能成为临床防治AS，以及促进缺血/再灌注心肌修复的新靶点。
Cell focal apoptosis is a newly discovered process of apoptosis, which involves the activation and degradation of various cytokines. First, intracellular inflammasome is activated, which in turn induces the activation of caspase-1 and the degradation of the proinflammatory cytokines IL-1 and IL-18 precursors. Thereafter, cell membrane fragmentation and nuclear DNA fragmentation can lead to the release of IL-1 and IL-18, eventually inducing an inflammatory response. The innate immune cells recognize the pathogen-related molecular patterns or damage-related molecular patterns by pattern recognition of receptors, induce apoptosis and eliminate the pathogen or damage tissue cells, forming an effective barrier to protect the body. More and more researches have shown that cell apoptosis is not only involved in the formation of atherosclerotic plaque in the pathological process of atherosclerosis (AS), but also an important factor that promotes plaque development and even affects plaque stability . In myocardial ischemia / reperfusion injury, cell apoptosis is also an important regulative factor of inflammatory reaction in MI and border areas, which may affect MI area, fibrosis and cardiac function during repair. Therefore, cell apoptosis may become a new target of clinical prevention and treatment of AS, as well as promote myocardial repair of ischemia / reperfusion.