Abstract
Besides its established function in erythropoiesis, erythropoietin (EPO) is currently also appreciated for its neuroprotective effects. The detrimental sequelae of prolonged cerebral hypoxia and ischemia have been shown to attenuate by EPO treatment. After binding to the EPO receptor, EPO is capable of initiating a cascade of events which--via different pathways--may lead to neuroprotection. The circumstances that determine which specific signalling route(s) are activated by EPO are largely unknown. We aim to provide the reader with a timely overview on the use of EPO in models of stroke and hypoxia-ischemia and to discuss the molecular events that underlie its neuroprotection.
Original language | English |
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Pages (from-to) | 22-33 |
Number of pages | 12 |
Journal | Brain Research Reviews |
Volume | 59 |
Issue number | 1 |
DOIs | |
Publication status | Published - Nov 2008 |
Keywords
- Animals
- Disease Models, Animal
- Erythropoietin/metabolism
- Humans
- Hypoxia-Ischemia, Brain/prevention & control
- Neuroprotective Agents/therapeutic use
- Signal Transduction/drug effects
- Time Factors