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Erythropoietin as a novel neuroprotectant

Genc S, Koroglu TF, Genc K2004PubMedJournal Article
PubMed
Neurological

Abstract

PURPOSE: To provide an overview of the current knowledge on neuroprotective properties of Erythropoietin (Epo), mechanisms by which Epo produces neuroprotection, and signaling pathways regulated by Epo in the nervous system. METHODS: The Medline database was searched for articles on the neuroprotective properties of Epo. Experimental and clinical studies were systematically reviewed. RESULTS: In addition to promoting the survival, proliferation, and differentiation of immature erythroid cells, Epo and the Epo receptor (EpoR) have recently been shown to exist and function in the nervous system. The Epo/EpoR system plays a critical role in neurodevelopment and neuroprotection. Epo ameliorates or prevents neuronal injury by neuroprotective, anti-apoptotic, anti-inflammatory, anti-oxidant, angiogenic, neurogenic and neurotrophic effects in cell culture and animal models of neurological diseases. The clinical effectiveness of recombinant human Epo in ischemic stroke in human patients has also been reported recently. CONCLUSION: Recent studies suggest that Epo is a potential novel neurotherapeutic agent and further clinical studies are warranted.

Cited By (4)

  • New avenues of exploration for erythropoietinJAMA · 2005
  • Erythropoietin in the brain: can the promise to protect be fulfilled?Trends in Pharmacological Sciences · 2004
  • Intrastriatal administration of erythropoietin protects dopaminergic neurons and improves neurobehavioral outcome in a rat model of Parkinson’s diseaseNeuroscience · 2007
  • Erythropoietin on a tightrope: balancing neuronal and vascular protection between intrinsic and extrinsic pathwaysNeurosignals · 2004

References (12)

  • Erythropoietin selectively attenuates cytokine production and inflammation in cerebral ischemia by targeting neuronal apoptosisThe Journal of Experimental Medicine · 2003
  • Erythropoietin fosters both intrinsic and extrinsic neuronal protection through modulation of microglia, Akt1, Bad, and caspase‐mediated pathwaysBritish Journal of Pharmacology · 2003

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