线粒体在运动保护心肌免受缺血再灌注损伤中的作用  

Role of Mitochondria in Exercise Protecting Myocardium From Ischemia-reperfusion Injury

作　　者：姬卫秀 耿燚 王硕 赵云罡[1] JI Wei-Xiu;GENG Yi;WANG Shuo;ZHAO Yun-Gang(Tianjin Key Laboratory of Exercise Physiology and Sports Medicine,Tianjin University of Sport,Tianjin 301617,China)

机构地区：[1]天津体育学院天津市运动生理学与运动医学重点实验室,天津301617

出　　处：《生物化学与生物物理进展》2024年第5期1090-1104,共15页Progress In Biochemistry and Biophysics

基　　金：国家自然科学基金(31971100);天津市教委科研计划(2019KJ114)资助项目。

摘　　要：线粒体是参与心肌缺血再灌注(myocardial ischemia and reperfusion,MI/R)损伤的关键细胞器,线粒体活性氧(reactive oxygen species,ROS)爆发、Ca2+失调、线粒体通透性转换孔(mitochondrial permeability transition pore,mPTP)开放、线粒体肿胀、促凋亡蛋白释放等都会导致线粒体功能障碍,心肌功能受损。运动是预防MI/R损伤的有效干预手段,其保护作用可能通过线粒体来实现。运动保护MI/R损伤的线粒体机制由多种因素决定,如线粒体能量学、KATP通道、mPTP、线粒体跨膜电位(ΔΨm)、线粒体蛋白、线粒体脂质、线粒体质量控制、远程调控因子等。本文综述了MI/R产生的线粒体机制,运动对MI/R的保护作用以及线粒体在其中的作用,以期为MI/R损伤的线粒体治疗策略提供参考。Acute myocardial infarction(AMI)has become the leading cause of death in cardiovascular diseases.Myocardial ischemia and reperfusion(MI/R)occurs when myocardial blood circulation is reconstructed after blood supply is limited or lack,often after myocardial infarction,and is the main cause of acute myocardial injury.According to the length of ischemia time,arrhythmia,myocardial inhibition,and myocardial infarction may occur in sequence in MI/R.Mitochondria are the key organelles involved in MI/R injury.Mitochondrial ROS eruption,Ca^(2+)imbalance,mPTP opening,mitochondrial swelling,and release of pro-apoptotic proteins all lead to mitochondrial dysfunction and myocardial function impairment.Exercise is an effective intervention to prevent myocardial ischemia-reperfusion injury,and its protective effect is closely related to the intensity of exercise,the length of exercise time,the type of exercise and the internal exercise ability.The mitochondrial mechanism of exercise protection against myocardial ischemia-reperfusion injury is determined by many factors.During reperfusion,the heart after trained is better able to maintain energy homeostasis,maintain ΔΨ_(m) and limit mPTP activation,maintain ATP synthesis.Activation of the sarcoKATP and/or mitoKATP channels by exercise induces cellular and/or myocardial hyperpolarization,protecting the mitochondria and myocardium during MI/R.Exercise-trained hearts can regulate calcium homeostasis during MI/R and limit mitochondrial Ca^(2+)overload.Exercise training can improve the activity of mitochondrial antioxidant enzymes to clear ROS and regulate mitochondrial Ca^(2+)concentration during MI/R.Exercise can increase the bioavailability of NO near mitochondria and indirectly achieve exercise-induced myocardial protection through protein S-nitrosylation and the eNOS-NO pathway is related to mitochondrial biogenesis after exercise training.Exercise training can also affect mitochondrial dynamics during MI/R by preventing mitochondrial division and promoting mitochondrial fusio

关 键 词：运动 线粒体 心肌缺血再灌注 

分 类 号：Q5[生物学—生物化学] Q7