Pathogenesis of retinopathy of prematurity

Acta Paediatr Suppl. 2002;91(437):26-8. doi: 10.1111/j.1651-2227.2002.tb00157.x.


Retinopathy of prematurity (ROP) is a blinding disease, initiated by delayed retinal vascular growth after premature birth. There are both oxygen-regulated and non-oxygen-regulated factors, which contribute to both normal vascular development and retinal neovascularization. One important oxygen-regulated factor, critical to both phases of ROP, is vascular endothelial growth factor (VEGF). A critical non oxygen-regulated growth factor is insulin-like growth factor (IGF-1). In knockout mice, lack of IGF-1 prevents normal retinal vascular growth, despite the presence of VEGF, important to vessel development. In vitro, low IGF-1 prevents vascular endothelial growth factor-induced activation of Akt, a kinase critical for vascular endothelial cell survival. Premature infants who develop ROP have lower levels of serum IGF-1 than age-matched infants without disease.

Conclusion: IGF-1 is critical to normal vascular development. Low IGF-1 predicts ROP and restoration of IGF-1 to normal levels may prevent ROP.

Publication types

  • Review

MeSH terms

  • Animals
  • Case-Control Studies
  • Disease Models, Animal
  • Endothelial Growth Factors / analysis
  • Endothelial Growth Factors / metabolism*
  • Endothelium, Vascular / cytology
  • Humans
  • Infant, Newborn
  • Infant, Premature*
  • Insulin-Like Growth Factor I / analysis
  • Insulin-Like Growth Factor I / metabolism*
  • Mice
  • Mice, Knockout
  • Prognosis
  • Retinal Vessels / metabolism
  • Retinal Vessels / physiopathology
  • Retinopathy of Prematurity / etiology
  • Retinopathy of Prematurity / physiopathology*
  • Risk Factors


  • Endothelial Growth Factors
  • Insulin-Like Growth Factor I