Myocardial ischemia is the leading cause of all cardiovascular deaths in North America. Myocardial ischemia is accompanied by profound changes in metabolism including alterations in glucose and fatty acid metabolism, increased uncoupling of glucose oxidation from glycolysis and accumulation of protons within the myocardium. These changes can contribute to a poor functional recovery of the heart. One key player in the ischemia-induced alteration in fatty acid and glucose metabolism is 5'AMP-activated protein kinase (AMPK). Accumulating evidence suggest that activation of AMPK during myocardial ischemia both increases glucose uptake and glycolysis while also increasing fatty acid oxidation during reperfusion. Gain-of-function mutations of AMPK in cardiac muscle may also be causally related to the development of hypertrophic cardiomyopathies. Therefore, a better understanding of role of AMPK in cardiac metabolism is necessary to appropriately modulate its activity as a potential therapeutic target in treating ischemia reperfusion injuries. This review attempts to update some of the recent findings that delineate various pathways through which AMPK regulates glucose and fatty acid metabolism in the ischemic myocardium.

中文翻译：

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AMP激活的蛋白激酶（AMPK）控制缺血性心脏中的脂肪酸和葡萄糖代谢。

在北美，心肌缺血是所有心血管疾病死亡的主要原因。心肌缺血伴随着新陈代谢的深刻变化，包括葡萄糖和脂肪酸代谢的改变，葡萄糖氧化与糖酵解的解偶联增加以及心肌内质子的积累。这些变化可导致心脏功能恢复不良。5'AMP激活的蛋白激酶（AMPK）是缺血引起的脂肪酸和葡萄糖代谢改变的关键因素。越来越多的证据表明，心肌缺血期间AMPK的激活既增加了葡萄糖的摄取和糖酵解，又增加了再灌注过程中的脂肪酸氧化。心肌中AMPK的功能获得性突变也可能与肥厚型心肌病的发展有因果关系。因此，需要更好地了解AMPK在心脏代谢中的作用，以适当调节其作为治疗缺血再灌注损伤的潜在治疗靶标的活性。这篇综述试图更新一些最近的发现，这些发现描述了AMPK调节缺血心肌中葡萄糖和脂肪酸代谢的各种途径。