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Cellular basis of uraemic cardiomyopathy: a role for erythropoietin?

机译:尿毒症心肌病的细胞基础:促红细胞生成素的作用?

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The use of erythropoietin (EPO) has revolutionized the treatment of anaemia associated with many conditions including chronic kidney disease (CKD). However, little is known of the cellular impact of EPO on the uraemic heart. The discovery that the EPO receptor (EPOR) is also expressed on non-haematopoietic cells including cardiomyocytes highlights a role of EPO beyond haematopoiesis. Animal models of heart failure have shown EPO can potentially reverse cardiac remodelling and improve myocardial function. Damage to the kidney, during uraemia, results in a decreased EPO production, which may render the uraemic heart more susceptible to damage and heart failure. Here we review current data on the cellular actions of EPO in models of left ventricular hypertrophy and heart failure and highlight parallels with the uraemic heart.
机译:促红细胞生成素(EPO)的使用彻底改变了与包括慢性肾脏病(CKD)在内的许多疾病相关的贫血的治疗方法。然而,关于EPO对尿毒症心脏的细胞影响知之甚少。 EPO受体(EPOR)也在包括心肌细胞在内的非造血细胞上表达的发现突出了EPO在造血功能之外的作用。心力衰竭的动物模型显示EPO可能会逆转心脏重塑并改善心肌功能。在尿毒症中,对肾脏的损害导致EPO生成减少,这可能使尿毒症心脏更容易受到损害和心力衰竭。在这里,我们审查有关左心室肥大和心力衰竭模型中EPO的细胞作用的当前数据,并强调与尿毒症心脏的相似之处。

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