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Cardiovascular Research 2006 71(3):408-410; doi:10.1016/j.cardiores.2006.06.007
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Copyright © 2006, European Society of Cardiology

Dissecting out the mechanism of cardioprotection by endogenous erthyropoietin using genetic engineering

Sean M. Davidson and Derek M. Yellon*

The Hatter Cardiovascular Institute, Royal Free and University College Medical School, Department of Medicine, 67 Chenies Mews, University College Hospital, London WC1E 6HX, United Kingdom

* Corresponding author. Tel.: +44 207 380 9591; fax: +44 207 388 5095. Email address: d.yellon@ucl.ac.uk

Received 30 May 2006; accepted 6 June 2006

The first 10% of the full text of this article appears below.

See article by Tada et al. [2] (pages 466–477) in this issue.

Erythropoietin (EPO), as the name suggests, was first discovered as a cytokine for red blood cells, but as is so often the case, turns out to have other highly interesting physiological effects. It is produced primarily in the kidneys, and its synthesis increases in response to a decrease in blood oxygen levels. In 1989, the use of recombinant EPO was approved for the treatment of anemia resulting from chronic renal failure. Anemia also occurs quite frequently in patients with chronic heart failure, and may be an independent risk factor for adverse outcomes [1]. Preliminary data suggests that treatment with EPO may improve symptoms . . . [Full Text of this Article]


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