摘要:
HM(hibernating myocardium)is an adaptive phenome-non of myocardium against sustained ischemia,which maintains its tissue vitality through balancing energy supply and demand.It widely exists in patients suffering from coronary heart disease. HMhas its own metabolic pattern,instead of regular FAO(fatty acid β-oxidation)-based metabolism,glycolysis became main pro-cedure.Reduction of FAO,TCA (tricarboxylic cacidcycle),ETC (electron transport chain)enzyme has been observed,ROS(reac-tive oxygen species)and UCP2(uncoupling protein 2)have been up-regulated.UCP2,which promotes proton leak across innermembrane of mitochondrial and leads to ATP reduction,has e-merged as an important regulator of the energy production.It is regulated by up-stream proteins such as AMPK,PPARs,PGC-1α,and other factors like FFA(free fat acid),ROS and purine nucleotide.HM has potential function of ischemic myocardium, which can improve cardiac function through reasonable interven-tion.Modulation of UCP2 can optimize energy production,and is essential to HM metabolism.%冬眠心肌是处于低灌注、低功能状态的一种自我保护心肌,心肌在低灌注状态下建立了心肌产能和耗能的平衡以维持心肌的存活性.冬眠心肌广泛存在于冠心病患者中,其底物代谢模式由脂肪酸代谢为主转变为以糖酵解为主的代谢模式,脂肪酸氧化、三羧酸循环、电子传递链相关酶均减低,活性氧簇(reactive oxygen species,ROS)生成增多,解偶联蛋白(uncoupling protein 2,UCP2)表达增高,能量代谢出现障碍,其中U C P2是位于线粒体内膜的质子转运体,是一种"质子漏",即质子不经过ATP合成酶(adenosine triphosphate synthase,ATP)而直接经过UCP2进入线粒体基质,导致的氧化磷酸化的解偶联,引起ATP生成的减少,能量代谢的障碍导致了心肌收缩功能减低.U C P2的表达受因上游蛋白、脂肪酸、ROS、嘌呤核苷酸的调控.通过调控UCP2可以增加冬眠心肌的产能,影响冬眠心肌的能量代谢.