Beta-lapachone inhibits pathological retinal neovascularization in oxygen-induced retinopathy via regulation of HIF-1α

Sung Wook Park, Jin Hyoung Kim, Ko Eun Kim, Moon Hee Jeong, Hyunsung Park, Bongju Park, Young Ger Suh, Woo Jin Park, Jeong Hun Kim

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24 Scopus citations


Retinal neovascularization in retinopathy of prematurity (ROP) is the most common cause of blindness for children. Despite evidence that hypoxia inducible factor (HIF)-1α -VEGF axis is associated with the pathogenesis of ROP, the inhibitors of HIF-1α have not been established as a therapeutic target in the control of ROP pathophysiology. We investigated the hypothesis that degradation of HIF-1α as a master regulator of angiogenesis in hypoxic condition, using β-lapachone, would confer protection against hypoxia-induced retinopathy without affecting physiological vascular development in mice with oxygen-induced retinopathy (OIR), an animal model of ROP. The effects of β-lapachone were examined after intraocular injection in mice with OIR. Intraocular administration of β-lapachone resulted in significant reduction in hypoxia-induced retinal neovascularization without retinal toxicity or perturbation of developmental retinal angiogenesis. Our results demonstrate that HIF-1α-mediated VEGF expression in OIR is associated with pathological neovascularization, not physiological angiogenesis. Thus, strategies blocking HIF-1α in the developing eye in the pathological hypoxia could serve as a novel therapeutic target for ROP.

Original languageEnglish
Pages (from-to)875-884
Number of pages10
JournalJournal of Cellular and Molecular Medicine
Issue number5
StatePublished - May 2014


  • Hypoxia-induced factor 1-α
  • Oxygen-induced retinopathy
  • Retinal neovascularization
  • Retinopathy of prematurity
  • Vascular endothelial growth factor
  • β-lapachone


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