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Timed topical dexamethasone eye drops improve mitochondrial function to prevent severe retinopathy of prematurity
Hitomi Yagi1, Myriam Boeck1, Mariya Petrishka-Lozenska2
1Boston Children's Hospital.
Insights
Topical dexamethasone eye drops, given early, can prevent retinopathy of prematurity (ROP) neovascularization in infants and mice. This early intervention targets mitochondrial function, offering a novel preventative strategy for ROP.
Area of Science:
- Ophthalmology
- Neonatology
- Molecular Biology
Background:
- Retinopathy of prematurity (ROP) causes visual impairment in preterm infants due to pathological neovascularization.
- Current ROP treatments are reactive, costly, and associated with severe complications.
Purpose of the Study:
- To evaluate the preventative efficacy of early topical dexamethasone for ROP.
- To investigate the underlying mechanisms of dexamethasone's action on retinal neovascularization.
Main Methods:
- Administered topical 0.1% dexamethasone in extremely preterm infants and a mouse oxygen-induced retinopathy (OIR) model.
- Assessed neovascularization, retinal mitochondrial gene expression, and inflammatory markers.
- Investigated the role of mitochondrial ATP synthetase.
Main Results:
- Early topical dexamethasone prevented ROP neovascularization in infants and suppressed it by 30% in OIR.
- Optimal timing was crucial; late treatment showed limited efficacy or exacerbated disease.
- Dexamethasone increased mitochondrial gene expression and decreased inflammatory markers, with effects reversed by blocking ATP synthetase.
Conclusions:
- Early topical dexamethasone is a promising preventative treatment for ROP.
- Dexamethasone's efficacy involves modulation of mitochondrial function and inflammatory pathways.
- This approach offers a simple, potentially preventative clinical strategy for severe ROP.
Abstract:
Pathological neovascularization in retinopathy of prematurity (ROP) can cause visual impairment in preterm infants. Current ROP treatments which are not preventative and only address late neovascular ROP, are costly and can lead to severe complications. We showed that topical 0.1% dexamethasone eye drops administered prior to peak neovessel formation prevented neovascularization in five extremely preterm infants at high risk for ROP and suppressed neovascularization by 30% in mouse oxygen-induced retinopathy (OIR) modeling ROP. In contrast, in OIR, topical dexamethasone treatment before any neovessel formation had limited efficacy in preventing later neovascularization, while treatment after peak neovessel formation had a non-statistically significant trend to exacerbating disease. Optimally timed topical dexamethasone suppression of neovascularization in OIR was associated with increased retinal mitochondrial gene expression and decreased inflammatory marker expression, predominantly found in immune cells. Blocking mitochondrial ATP synthetase reversed the inhibitory effect of dexamethasone on neovascularization in OIR. This study provides new insights into topical steroid effects in retinal neovascularization and into mitochondrial function in phase II ROP, and suggests a simple clinical approach to prevent severe ROP.
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