心肌缺血再灌注损伤(MIRI)的发生机制至今仍未完全阐明，针对现有机制采取的措施尚未取得理想的心肌保护作用，所以进一步深入研究其机制和寻找新的治疗靶点至关重要。线粒体功能障碍与心肌细胞能量代谢紊乱、心肌细胞坏死和凋亡的关系密切，在MIRI的发生发展中起到关键调节作用。本文主要阐述了线粒体动力学、自身线粒体输注、心磷脂、线粒体通透性转换孔和线粒体三磷酸腺苷敏感性钾离子通道与MIRI的关系，为进一步研究MIRI发生机制，制定防治措施提供新的方向和思路。“,”The mechanism of myocardial ischemia-reperfusion injury (MIRI) has not been fully elucidated nowadays, and the measures which are taken based on the existing mechanism have not achieved ideal myocardial protection effects. Therefore, it is crucial to further deepen its mechanism research and find new therapeutic targets. Mitochondrial dysfunction is closely related to myocardial energy metabolism disorder, myocardial cell necrosis and apoptosis, and it plays a key regulatory role in the occurrence and development of MIRI. This review has mainly elaborated the relationship between MIRI and mitochondrial kinetics, autologous mitochondria transplantation, cardiolipin, mitochondrial permeability transition pore and mitochondrial adenosine triphosphate (ATP)-sensitive potassium channel, thereby providing new directions and ideas to develop remedy for MIRI in the future.