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Erythropoietin: ready for prime-time cardioprotection.

机译:促红细胞生成素:准备进行黄金时段的心脏保护。

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摘要

To improve clinical outcomes in patients presenting with an acute myocardial infarction, new strategies to limit infarct size and postinfarct remodelling are warranted. Recent animal studies have revealed that erythropoietin has the potential to achieve both these goals. Even more intriguing is the possibility that erythropoietin could protect the myocardium when administered well after the onset of reperfusion. In this article we review the evidence in favour of erythropoietin-induced cardioprotection and the proposed underlying mechanisms. Inhibition of apoptosis and inflammation, as well as stimulation of neovascularization, all could contribute to cardioprotection. Activation of the reperfusion injury salvage kinase pathway at the moment of reperfusion appears to be a pivotal mechanism in the infarct size-limiting effect. Now that recent evidence has proven that erythropoietin also can protect the human heart, studies currently are being undertaken to examine the effect of administration of erythropoietin in patients presenting with an acute myocardial infarction.
机译:为了改善急性心肌梗死患者的临床结局,必须采取新的策略来限制梗死面积和梗死后重塑。最近的动物研究表明,促红细胞生成素有可能实现这两个目标。更令人感兴趣的是,在再灌注开始后良好使用时,促红细胞生成素可以保护心肌。在本文中,我们回顾了促红细胞生成素诱导的心脏保护作用和拟议的潜在机制的证据。抑制细胞凋亡和炎症,以及刺激新血管形成,都可以促进心脏保护。在再灌注时激活再灌注损伤抢救激酶途径似乎是梗死面积限制作用的关键机制。既然最近的证据已经证明促红细胞生成素也可以保护人的心脏,目前正在进行研究以研究在患有急性心肌梗塞的患者中应用促红细胞生成素的效果。

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