When Müller cells are exposed to high oxygen, not only is their capacity to produce glutamine decreased, but they start to consume glutamine themselves. This may be the primary mechanism of retinopathy of prematurity.
Administration of the HIF stabilizer roxadustat during hyperoxia does not result in pathological angiogenesis, and instead effectively prevents oxygen-induced retinopathy, Cleveland Clinic researches have determined using a mouse model.
Hear about Cleveland Clinic’s latest ophthalmology research and treatment insights by attending these presentations at booth 713.
The promise of systemic therapy for retinopathy of prematurity lies in simultaneous protection of multiple organs from oxygen toxicity, helping to promote normal, sequential development of blood vessels in premature tissues.
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Low-dose, systemic, intermittent drug delivery tested in animal model as way to alleviate hyperoxia-induced retinal damage in ROP.