线粒体动力学在心肌缺血/再灌注损伤中的研究进展

Research Progress in Mitochondrial Dynamics and the Functional Roles in Myocardial Ischemia/Reperfusion Injury

线粒体稳态是机体在代谢或者环境应激反应中维持心脏功能的关键。线粒体动力学(分裂、融合)在维持线粒体稳态中发挥重要作用,其过程主要由线粒体动力学相关蛋白介导。心肌缺血/再灌注损伤时,活性氧类大量产生及Ca2+超载,导致线粒体通透性转换孔开放、线粒体膜电位降低,最终导致细胞凋亡。研究表明活性氧类和Ca2+超载会通过介导线粒体动力学蛋白从而调控线粒体融合和分裂。该文综述了线粒体动力学相关分子在心肌缺血/再灌注损伤中的研究进展,以期为心血管疾病的治疗提供潜在的治疗靶点。

Mitochondrial homeostasis is critical for keeping cardiac function in response to metabolic or environmental stresses.Mitochondrial dynamics(fission and fusion)play essential roles in maintaining mitochondrial homeostasis,which is determined by mitochondrial fission and fusion proteins.Ischemia/reperfusion injury of the heart is characterized by Ca 2+overload and a burst of reactive oxygen species generation at the onset of reperfusion which result in mitochondrial permeability transition pore opening,mitochondrial membrane potential decrease and finally apoptosis.Reactive oxygen species and Ca 2+overload significantly contribute to mitochondrial fission and fusion via the modulation of mitochondrial dynamics proteins.Here is to make an overview of mechanisms of mitochondrial dynamics regulation in myocardial ischemia/reperfusion injury to provide potential therapeutic targets for treating cardiovascular diseases.