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Updated: Jul 16, 2026
Monitoring Dynamic Growth of Retinal Vessels in Oxygen-Induced Retinopathy Mouse Model
Published on: April 2, 2021
Retinopathy of prematurity
1Department of Ophthalmology, Harvard Medical School and Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, USA.
Insights
Retinopathy of prematurity (ROP) is a blinding disease in premature infants. Restoring insulin-like growth factor 1 (IGF-1) levels may prevent ROP by regulating pathological vessel growth.
Area of Science:
- Ophthalmology
- Neonatology
- Developmental Biology
Background:
- Retinopathy of prematurity (ROP) is a leading cause of childhood blindness, affecting both developed and developing nations.
- ROP involves two phases: initial delayed retinal vascularization and subsequent hypoxia-driven pathological neovascularization.
- Key risk factors include oxygen exposure and premature birth, impacting vascular endothelial growth factor (VEGF) regulation.
Purpose of the Study:
- To investigate the role of insulin-like growth factor 1 (IGF-1) in the pathogenesis of retinopathy of prematurity.
- To explore the relationship between serum IGF-1 levels and ROP severity in premature infants.
- To determine if IGF-1 modulation could be a therapeutic strategy for ROP.
Main Methods:
- Serum IGF-1 levels were measured in premature infants.
- Correlation between IGF-1 levels and clinical ROP severity was assessed.
- The interaction between IGF-1 and VEGF in retinal neovascularization was examined.
Main Results:
- Serum IGF-1 levels in premature infants directly correlated with ROP severity.
- IGF-1 acts as a permissive factor, enabling VEGF-stimulated vessel growth.
- Lack of IGF-1 impairs normal retinal vascularization in phase I, while rising levels in phase II promote pathological neovascularization.
Conclusions:
- IGF-1 plays a critical, non-oxygen-regulated role in ROP development.
- Serum IGF-1 levels are a significant indicator of ROP progression.
- Restoring IGF-1 levels in preterm infants may offer a novel approach to preventing ROP.
Abstract:
Retinopathy of prematurity (ROP) is a common blinding disease in children in the developed world despite current treatment, and is becoming increasingly prevalent in the developing world. ROP progresses in two phases. The first phase begins with delayed retinal vascular growth after birth and partial regression of existing vessels, followed by a second phase of hypoxia-induced pathological vessel growth. Two major risk factors of ROP are the use of oxygen and a decreased gestation period. Excessive oxygen contributes to ROP through regulation of vascular endothelial growth factor (VEGF). Suppression of VEGF by oxygen in phase I of ROP inhibits normal vessel growth, whereas elevated levels of VEGF induced by hypoxia in phase II of ROP precipitate pathological vessel proliferation. Insulin-like growth factor 1 (IGF-1) is a critical non-oxygen-regulated factor in ROP. We have found that serum levels of IGF-1 in premature babies directly correlate with the severity of clinical ROP. IGF-1 acts indirectly as a permissive factor by allowing maximal VEGF stimulation of vessel growth. Lack of IGF-1 in preterm infants prevents normal retinal vascular growth in phase I of ROP, despite the presence of VEGF. As infants mature, rising levels of IGF-1 in phase II of ROP allows VEGF stimulated pathological neovascularization. These findings suggest that restoration of IGF-1 to normal levels might be useful in preventing ROP in preterm infants.
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