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European Journal of Heart Failure 2009 11(8):732-738; doi:10.1093/eurjhf/hfp093
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Cellular basis of uraemic cardiomyopathy: a role for erythropoietin?

Katie Smith1, David Semple1, Sunil Bhandari2 and Anne-Marie L. Seymour1,*

1 Department of Biological Sciences, Hull York Medical School, University of Hull, Kingston-upon-Hull HU6 7RX, UK
2 Department of Renal Medicine, Hull and East Yorkshire Hospital NHS Trust, Kingston-upon-Hull, UK

* Corresponding author. Tel: +44 14824 65517, Fax: +44 14824 65458, Email: a.m.seymour{at}hull.ac.uk


  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.

Key Words: Uraemic cardiomyopathy • Erythropoietin • Left ventricular hypertrophy • Remodelling

Received December 30, 2008; Revised April 29, 2009; Accepted May 18, 2009


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