Riksen Niels P, Hausenloy Derek J, Yellon Derek M
The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London WC1E 6HX, United Kingdom.
Trends Pharmacol Sci. 2008 May;29(5):258-67. doi: 10.1016/j.tips.2008.02.002. Epub 2008 Mar 21.
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.
为改善急性心肌梗死患者的临床预后，有必要采取新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，在再灌注开始后很长时间给予促红细胞生成素，它仍有可能保护心肌。在本文中，我们综述了支持促红细胞生成素诱导心脏保护作用的证据及其潜在机制。抑制细胞凋亡和炎症以及刺激新血管形成，都可能有助于心脏保护。再灌注时再灌注损伤挽救激酶途径的激活似乎是梗死面积限制效应的关键机制。鉴于最近的证据已证明促红细胞生成素也能保护人类心脏，目前正在进行研究以检验在急性心肌梗死患者中给予促红细胞生成素的效果。
