A novel protective effect of erythropoietin in the infarcted heart
A novel protective effect of erythropoietin in the infarcted heart
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DOI：
10.1172/jci200318200
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发表时间：
2003-10-01
影响因子：
15.9
通讯作者：
Koch, WJ
中科院分区：
文献类型：
--
作者：
Parsa, CJ;Matsumoto, A;Koch, WJ
促红细胞生成素（EPO）已被证明可以保护神经元免受缺血性中风，但也可以增加缺血性心脏病患者的血栓形成事件和死亡率。我们推断EPO的益处可能被红细胞压积的增加所抵消，并评估了EPO在缺血性心脏中的直接作用。我们发现，EPO预处理可保护体外H9c2成肌细胞和体内心肌细胞免受缺血损伤。EPO治疗可显著改善心肌梗死后的心脏功能。这种保护作用与减轻心肌细胞凋亡有关，转化为更有活力的心肌和更少的心室功能障碍。EPO介导的心肌细胞存活似乎涉及Akt激活。重要的是，EPO的心脏保护作用在没有红细胞比容增加的情况下被观察到（消除氧递送作为肌细胞存活和功能的病因因素），这表明EPO可以直接保护缺血和梗死的心脏。
Erythropoietin (EPO) has been shown to protect neurons from ischemic stroke, but can also increase thrombotic events and mortality rates in patients with ischemic heart disease. We reasoned that benefits of EPO might be offset by increases in hematocrit and evaluated the direct effects of EPO in the ischemic heart. We show that preconditioning with EPO protects H9c2 myoblasts in vitro and cardiomyocytes in vivo against ischemic injury. EPO treatment leads to significantly improved cardiac function following myocardial infarction. This protection is associated with mitigation of myocyte apoptosis, translating into more viable myocardium and less ventricular dysfunction. EPO-mediated myocyte survival appears to involve Akt activation. Importantly, cardioprotective effects of EPO were seen without an increase in hematocrit (eliminating oxygen delivery as an etiologic factor in myocyte survival and function), demonstrating that EPO can directly protect the ischemic and infarcted heart.