线粒体通透转换孔与心肌缺血-再灌注损伤  

Mitochondrial permeability transition pore and myocardial ischemia-reperfusion injury

作　　者：刘晓明[1] 徐建国[1] 

机构地区：[1]南京军区南京总医院南京大学医学院临床学院麻醉科,江苏南京210002

出　　处：《医学研究生学报》2007年第3期327-330,共4页Journal of Medical Postgraduates

基　　金：南京军区南京总医院科研基金资助项目(批准号:2004045)

摘　　要：缺血-再灌注会导致线粒体通透转换孔(MPTP)的开放,通道的低水平开放和随后的关闭,会导致线粒体释放细胞色素C及其他前凋亡分子,如果开放无限制继续,会导致离子稳态失衡,引起一系列细胞死亡的瀑布式反应。缺血-再灌注期间直接或间接的抑制MPTP开放,对再灌注损伤产生明显的保护作用。近期发现,MPTP短暂的低水平开放对其后的再灌注损伤也有保护作用。作者着重对MPTP的组成及机制、心肌缺血-再灌注时的通透改变和与心肌缺血预处理的关系作一综述,以寻求防治心肌缺血-再灌注损伤的新策略。Ischemia-reperfusion of the heart leads to the opening of mitochondrial permeability transition pore （MPTP）. Transient opening and subsequent closure of the MPTP may lead to the release of cytochrome c and other proapoptotic molecules. If unrestrained, this will lead to the loss of ionic homeostasis and initiate the cascade of necrotic cell death. Direct or indirect inhibition of MPTP provides protection against ischemia-reperfusion injury. Recent researches have shown that transient low-conductance pore opening also provides protection against reperfusion injury. This review gives summarization of the components, molecular mechanism of MPTP, permeability transition in myocardial ischemia-reperfusion and the relationship between MPTP and ischemic preconditioning. This may lead to better protective strategies against myocardial ischemia-reperfusion injury in the future.

关 键 词：线粒体通透转换孔 缺血-再灌注损伤 心肌缺血预处理 

分 类 号：Q244[生物学—细胞生物学]