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Cardiovascular Research Advance Access originally published online on November 10, 2007
Cardiovascular Research 2008 77(1):2-3; doi:10.1093/cvr/cvm064
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Thrombopoietin emerges as a new haematopoietic cytokine that confers cardioprotection against acute myocardial infarction

John W. Calvert1 and David J. Lefer1,2,*

1 Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
2 Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA

* Corresponding author. Tel: +1 718 430 2645; fax: +1 718 430 8989. E-mail address: dlefer@aecom.yu.edu

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

Editorial commentary on ‘Human thrombopoietin reduces myocardial infarct size, apoptosis, and stunning following ischaemia/reperfusion in rats.’ (Baker et al. 4)

Colony stimulating factors (CSFs), also called haematopoietic growth factors, are circulating cytokines that regulate the bone marrow production of red cells, white cells, and platelets. CSFs have also been reported to act on stem cells to regulate lineage-specific differentiation.1 Erythropoietin (EPO) controls red cell production and has been utilized in recombinant form for the treatment of anaemia in patients with end-stage renal disease since 1988. Granulocyte CSF (G-CSF) acts on haematopoietic stem cells to regulate neutrophil progenitor proliferation and differentiation. G-CSF is routinely used to mobilize stem cells in normal patients for transplantation of cells into . . . [Full Text of this Article]


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Human thrombopoietin reduces myocardial infarct size, apoptosis, and stunning following ischaemia/reperfusion in rats
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