Ischemia reperfusion injury (I/R injury) contributes significantly to morbidity and mortality following myocardial infarction (MI). Although rapid reperfusion of the ischemic myocardium was established decades ago as a highly beneficial therapy for MI, significant cell death still occurs after the onset of reperfusion. Mitochondrial dysfunction is closely associated with I/R injury, resulting in the uncontrolled production of reactive oxygen species (ROS). Considerable efforts have gone into understanding the metabolic perturbations elicited by I/R injury. Recent work has identified the critical role of reversible protein acetylation in maintaining normal mitochondrial biologic function and energy metabolism both in the normal heart and during I/R injury. Several studies have shown that modification of class I HDAC and/or Sirtuin (Sirt) activity is cardioprotective in the setting of I/R injury. A better understanding of the role of these metabolic pathways in reperfusion injury and their regulation by reversible protein acetylation presents a promising way forward in improving the treatment of cardiac reperfusion injury. Here we briefly review some of what is known about how acetylation regulates mitochondrial metabolism and how it relates to I/R injury.

中文翻译：

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心脏缺血再灌注损伤中线粒体酶乙酰化对代谢的调节。

缺血再灌注损伤（I / R损伤）明显增加了心肌梗死（MI）的发病率和死亡率。尽管几十年前就建立了缺血心肌的快速再灌注作为MI的高度有益疗法，但在再灌注开始后仍会发生大量细胞死亡。线粒体功能障碍与I / R损伤密切相关，导致不受控制的活性氧（ROS）产生。在理解I / R损伤引起的代谢紊乱方面已经付出了巨大的努力。最近的工作已经确定了可逆蛋白乙酰化在维持正常心脏和I / R损伤过程中正常线粒体生物学功能和能量代谢中的关键作用。几项研究表明，改变I类HDAC和/或Sirtuin（Sirt）活性对I / R损伤具有心脏保护作用。更好地了解这些代谢途径在再灌注损伤中的作用及其通过可逆蛋白乙酰化的调控，为改善心脏再灌注损伤的治疗方法提供了一个有希望的途径。在这里，我们简要回顾一些有关乙酰化如何调节线粒体代谢及其与I / R损伤之间关系的已知知识。