急性心肌梗死缺血心肌线粒体蛋白组学的研究概况

Researches on Mitochondrial Proteomics of Acute Myocardial Infarction and Myocardial Ischemia

目的线粒体作为能量供应的核心细胞器,其结构的完整和功能的稳定对调控心肌细胞氧化应激、Ca^(2+)稳态和细胞凋亡至关重要,文章概述急性心肌梗死(acute myocardial infarction,AMI)后缺血心肌线粒体蛋白组学的临床和基础研究。方法以近年来AMI后缺血心肌线粒体损伤涉及的心肌再灌注损伤、无复流等蛋白组学的研究文献,概括线粒体蛋白组学的研究近况。结果AMI产生过量的活性氧和细胞内Ca^(2+)的积聚使心肌线粒体损伤导致心肌细胞处于缺能状态,最终引起心肌细胞的缺血、凋亡、坏死。随着AMI绿色通路的建立,冠状动脉旁路移植术、经皮冠状动脉介入治疗(PCI)等得到广泛应用,引起的心肌再灌注损伤、无复流等是临床面临的主要课题,缺血及再灌注后线粒体功能及结构明显受损,线粒体蛋白参与的三磷酸腺苷(ATP)合成和循环、脂肪酸氧化、氨基酸降解等过程发生障碍。结论AMI后及再灌注处理对心肌线粒体蛋白组学的变化,可从亚细胞水平揭示AMI及缺血后处理条件下心肌线粒体蛋白表达的变化和新的治疗靶点。

Objective As we all known,mitochondrion has been the primary organelle that participate in the energy production,whose structural integrity and functional stability are crucial to regulating oxidative stress,calcium homeostasis and cell apoptosis.There have been some clinical and basic researchs on proteomics about ischemic myocardial mitochondria post acute myocardial infarction,and we will give a review then.Methods According to recent documents on proteomics about myocardial reperfusion injury and no reflow post myocardial injury result from acute myocardial infarction.Results Excessive reactive oxygen species and calcium accumulation has been the major pathological changes during the processes of AMI.which lead myocardium to be energy deficiency,at last going necrosis and apoptosis.With the establishment of green channel for patients with acute myocardial infarction,more and more patients have access to coronary artery bypass grafting and percutaneous coronary intervention（PCI）,meanwhile,ischemia / reperfusion injury and no reflow have been the problem that clinicians have to recognize.Ischemia and reperfusion will lead to injury of the mitochondrial structure and function,further to hinder the processes of adenosine triphosphate（ATP） synthesis,three critic acid cycle,fatty acid oxidation,amino acid degradation.Conclusion To study the changes of myocardial mitochondrion proteomics post AMI and reperfusion treatment,we can reveal the protein expression difference from subcellular level and explore new therapeutic targets.