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尿毒症性心肌病的细胞基础:促红细胞生成素的作用?

Cellular basis of uraemic cardiomyopathy: a role for erythropoietin?

机构信息

Department of Biological Sciences, Hull York Medical School, University of Hull, Kingston-upon-Hull, UK.

出版信息

Eur J Heart Fail. 2009 Aug;11(8):732-8. doi: 10.1093/eurjhf/hfp093.

Abstract

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.

摘要

促红细胞生成素(EPO)的应用彻底改变了许多疾病相关贫血的治疗方法,包括慢性肾脏病(CKD)。然而,人们对 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 在造血之外的作用。心力衰竭的动物模型表明,EPO 可能潜在地逆转心脏重构并改善心肌功能。尿毒症期间肾脏损伤导致 EPO 产生减少,这可能使尿毒症心脏更容易受到损伤和心力衰竭的影响。在这里,我们回顾了左心室肥厚和心力衰竭模型中 EPO 的细胞作用的现有数据,并强调了与尿毒症心脏的相似之处。

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