NDT Advance Access originally published online on October 24, 2008
Nephrology Dialysis Transplantation 2009 24(2):388-390; doi:10.1093/ndt/gfn590
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Erythropoietin and microvascular diabetic complications*
Department of Nephrology and Hypertension, University of Erlangen-Nürnberg, Germany
Correspondence and offprint requests to: Kai-Uwe Eckardt, University Clinic Erlangen, Department of Medicine 4, Krankenhausstr. 12, 91054 Erlangen, Germany. Tel: +49-9131-85-39002; Fax: +49-9131-85-39209; E-mail: kai-uwe.eckardt@uk-erlangen.de
Keywords: anaemia; diabetic nephropathy; diabetic retinopathy; erythropoietin
| The first 150 words of the full text of this article appear below. |
When recombinant human erythropoietin (EPO) became available for clinical use, the hormone was considered as a specific erythropoietic growth factor and as a more or less unique molecule, since its endogenous production increases in response to reduced oxygen availability. Subsequently, we have witnessed a revolutionary increase in knowledge about the highly conserved ability of virtually all cells to sense oxygen and to translate reductions in oxygen availability into specific patterns of gene expression. This hypoxia response is to a large extent mediated by hypoxia-inducible transcription factors (HIF). EPO is the prime example for a hypoxia-inducible HIF target gene, but more than 100 additional genes have meanwhile also been identified as HIF targets, including genes involved in new vessel formation and anaerobic metabolism. In general, the activation of the hypoxia pathway stimulates responses that increase either oxygen availability or hypoxia tolerance [1].
Consistent with this broader perspective of oxygen
| Promoter polymorphism of the EPO gene in diabetic patients with retinopathy and ESRD |
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| Inconsistencies and open questions |
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| Clinical consequences? |
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