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Updated: May 12, 2026
Monitoring Dynamic Growth of Retinal Vessels in Oxygen-Induced Retinopathy Mouse Model
Published on: April 2, 2021
The pathophysiology of retinopathy of prematurity: an update of previous and recent knowledge
Giacomo Cavallaro1, Luca Filippi, Paola Bagnoli
1NICU, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico - Università degli Studi di Milano, Milan, ItalyNICU, Medical and Surgical Feto-Neonatal Department, "A. Meyer" University Children's Hospital, Florence, ItalyDepartment of Biology, Unit of General Physiology, University of Pisa, Pisa, ItalyNeurometabolic Unit, Department of Pediatric Neurosciences, "A. Meyer" University Children's Hospital, Florence, ItalyDepartment of Ophthalmology, Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy.
Insights
Retinopathy of prematurity (ROP) is a leading cause of infant blindness. New research explores pathophysiological mechanisms and novel therapies targeting vascular endothelial growth factors (VEGF) and genetic factors for improved ROP treatment.
Area of Science:
- Ophthalmology
- Neonatology
- Vascular Biology
Background:
- Retinopathy of prematurity (ROP) is a significant cause of blindness in premature infants, strongly linked to birth weight and gestational age.
- Current ROP therapies are insufficient, necessitating research into novel antivasculogenic treatments.
- Understanding ROP pathogenesis is crucial for developing effective interventions.
Purpose of the Study:
- To review pathophysiological mechanisms driving ROP progression.
- To investigate novel therapeutic strategies for ROP.
- To explore the roles of oxygen, growth factors, and genetic components in ROP.
Main Methods:
- Review of existing literature on ROP pathogenesis and therapies.
- Analysis of the roles of oxygen levels, hypoxia-inducible factor 1, and vascular endothelial growth factors (VEGF) in retinal angiogenesis.
- Examination of the involvement of Insulin-like Growth Factor 1 (IGF-1), Erythropoietin (Epo), and genetic factors like β-adrenergic receptors (β-ARs).
Main Results:
- Oxygen levels critically regulate retinal angiogenesis via hypoxia-inducible factor 1 and VEGF.
- IGF-1 and Epo influence ROP progression; rhIGF-1 and rhEpo showed potential in preventing vasculature loss, while anti-VEGF drugs target the proliferative phase.
- Genetic factors, including single-nucleotide polymorphisms in β-ARs, may play a role in ROP pathogenesis.
Conclusions:
- ROP pathogenesis involves complex interactions of oxygen, growth factors, and genetic elements.
- Emerging therapies targeting VEGF, IGF-1, Epo, and genetic pathways offer new hope for ROP treatment.
- Further research into these factors could lead to improved understanding and prevention of ROP-induced blindness.
Abstract:
Retinopathy of prematurity (ROP) is a disease that can cause blindness in very low birthweight infants. The incidence of ROP is closely correlated with the weight and the gestational age at birth. Despite current therapies, ROP continues to be a highly debilitating disease. Our advancing knowledge of the pathogenesis of ROP has encouraged investigations into new antivasculogenic therapies. The purpose of this article is to review the findings on the pathophysiological mechanisms that contribute to the transition between the first and second phases of ROP and to investigate new potential therapies. Oxygen has been well characterized for the key role that it plays in retinal neoangiogenesis. Low or high levels of pO2 regulate the normal or abnormal production of hypoxia-inducible factor 1 and vascular endothelial growth factors (VEGF), which are the predominant regulators of retinal angiogenesis. Although low oxygen saturation appears to reduce the risk of severe ROP when carefully controlled within the first few weeks of life, the optimal level of saturation still remains uncertain. IGF-1 and Epo are fundamentally required during both phases of ROP, as alterations in their protein levels can modulate disease progression. Therefore, rhIGF-1 and rhEpo were tested for their abilities to prevent the loss of vasculature during the first phase of ROP, whereas anti-VEGF drugs were tested during the second phase. At present, previous hypotheses concerning ROP should be amended with new pathogenetic theories. Studies on the role of genetic components, nitric oxide, adenosine, apelin and β-adrenergic receptor have revealed new possibilities for the treatment of ROP. The genetic hypothesis that single-nucleotide polymorphisms within the β-ARs play an active role in the pathogenesis of ROP suggests the concept of disease prevention using β-blockers. In conclusion, all factors that can mediate the progression from the avascular to the proliferative phase might have significant implications for the further understanding and treatment of ROP.
