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Updated: Oct 30, 2025

Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
Hyperoxia Inhibits Proliferation of Retinal Endothelial Cells in a Myc-Dependent Manner
Charandeep Singh1, Andrew Benos1, Allison Grenell1,2
1Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
Insights
High oxygen levels are vital for premature infants but can cause retinopathy of prematurity. This study reveals a new Myc-dependent pathway regulating cell growth that contributes to this condition.
Area of Science:
- Ophthalmology
- Neonatology
- Molecular Biology
Background:
- Oxygen supplementation is crucial for preventing mortality in premature infants.
- However, excessive oxygen can lead to retinopathy of prematurity (ROP), characterized by impaired retinal vascular development.
- The precise molecular mechanisms driving ROP remain incompletely understood.
Purpose of the Study:
- To investigate the role of hyperoxia in regulating retinal endothelial cell proliferation.
- To identify novel molecular pathways involved in oxygen-induced retinopathy.
Main Methods:
- Utilizing a mouse model to study the effects of hyperoxia on retinal development.
- Analyzing cell cycle regulation and endothelial cell proliferation in response to oxygen levels.
- Investigating the involvement of the Myc oncogene in these processes.
Main Results:
- Hyperoxia significantly alters cell cycle regulation in retinal endothelial cells.
- A previously unknown Myc-dependent pathway was identified as a key regulator of endothelial cell proliferation under hyperoxic conditions.
- This pathway contributes to the vaso-attenuation and vaso-obliteration characteristic of ROP.
Conclusions:
- Hyperoxia induces retinopathy of prematurity through a novel Myc-dependent regulation of the cell cycle and retinal endothelial cell proliferation.
- Targeting this Myc-dependent pathway may offer a therapeutic strategy for preventing or treating ROP in premature infants.
Abstract:
Oxygen supplementation is necessary to prevent mortality in severely premature infants. However, the supraphysiological concentration of oxygen utilized in these infants simultaneously creates retinovascular growth attenuation and vasoobliteration that induces the retinopathy of prematurity. Here, we report that hyperoxia regulates the cell cycle and retinal endothelial cell proliferation in a previously unknown Myc-dependent manner, which contributes to oxygen-induced retinopathy.

