title: Erythropoietin: when liability becomes asset in neurovascular repair.
abstract: Erythropoietin (Epo) leads to the proliferation and differentiation of erythroid precursors, but is also involved in diverse nonhematopoietic biological functions. In this issue of the JCI, Chen, Smith, and colleagues demonstrate that the temporal expression of Epo is critical for determining whether physiological or pathological repair occurs following neurovascular retinal injury in the oxygen-induced retinopathy neonatal mouse model (see the related article beginning on page 526). The pleiotrophic properties of Epo make it a likely novel therapy for treatment of neurovascular damage, but the timing of its use must be carefully considered to prevent untoward effects.
authors.affiliation: Program in Stem Cell Biology and Regenerative Medicine, Department of Pharmacology and Therapeutics, University of Florida, Gainesville, Florida 32610, USA. grantma@ufl.edu
authors.forename: Maria B
authors.initials: MB
authors.lastname: Grant
authors.forename: Michael E
authors.initials: ME
authors.lastname: Boulton
authors.forename: Alexander V
authors.initials: AV
authors.lastname: Ljubimov
mesh_terms: D000818:Animals; D015672:Erythroid Precursor Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D004921:Erythropoietin / Q000494:pharmacology / Q000502:physiology* / Q000627:therapeutic use*; D006801:Humans; D051379:Mice; D009389:Neovascularization, Pathologic / Q000188:drug therapy* / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D012164:Retinal Diseases / Q000188:drug therapy*
chemical_list: D018696:Neuroprotective Agents; D004921:Erythropoietin