© 2004 by European Society of Cardiology
Copyright © 2004, European Society of Cardiology
An update on the cardiac effects of erythropoietin cardioprotection by erythropoietin and the lessons learnt from studies in neuroprotection
Cell Signalling Laboratory, Biochemistry and Molecular Biology, School of Biomedical and Chemical Sciences, University of Western Australia, Australia-
Western Australian Institute for Medical Research, Australia
* Cell Signalling Laboratory, Biochemistry and Molecular Biology, School of Biomedical and Chemical Sciences, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia. Tel: +61-8-6488-1348; fax: +61-8-6488-1148. Email address: marieb{at}cyllene.uwa.edu.au
Erythropoietin (Epo) was once thought to act exclusively in the formation of red blood cells. As recently reviewed by Smith et al. [Cardiovasc. Res. 59 (2003) 538–548], Epo can also act within the cardiovascular system with effects in thrombosis and hypertension as well as actions on platelets, vascular endothelium and smooth muscle, and myocytes of the heart. Here, the actions of Epo to protect neuronal cells of the brain are first evaluated and parallel actions of Epo in cardioprotection are then drawn. Thus, with recent reports of Epo receptor (EpoR) expression by cardiac myocytes, it could be predicted that Epo initiates direct protective signalling events. This is supported by five independent studies published in 2003 showing Epo protects cardiac myocytes following ischemia/reperfusion. Importantly, these protective actions have been observed in vitro and in vivo. The former suggests the direct actions of Epo to prevent myocyte death independently of its effects on red blood cell number or cells other than cardiac myocytes. The latter demonstrates the potential for Epo in the treatment of the heart post-infarction, decreasing the numbers of apoptotic myocytes, limiting infarct expansion and attenuating the post-infarct deterioration in haemodynamic function. These beneficial effects of Epo should stimulate further research into the actions of Epo.
KEYWORDS Apoptosis; Phosphatidyl inositol 3' kinase; In vitro cardioprotection; In vivo cardioprotection; Ischemia/reperfusion damage
Time for primary review 29 days
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