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Whether long non-coding RNA myocardial infarction-associated transcript is involved in oxygen-induced retinopathy remains poorly understood.To validate this hypothesis,we established a newborn mouse model of oxygen-induced retinopathy by feeding in an oxygen concentration of 75 ± 2％from postnatal day 8 to postnatal day 12,followed by in normal air.On postnatal day 11,the mice were injected with the myocardial infarction-associated transcript siRNA plasmid via the vitreous cavity to knockdown long non-coding RNA myocardial infarction-associated transcript.Myocardial infarction-associated transcript siRNA transcription significantly inhibited myocardial infarction-associated transcript mRNA expression,reduced the phosphatidylinosital-3-kinase,phosphorylated Akt and vascular endothelial growth factor immunopositivities,protein and mRNA expression,and alleviated the pathological damage to the retina of oxygen-induced retinopathy mouse models.These findings suggest that myocardial infarction-associated transcript is likely involved in the retinal neovascularization in retinopathy of prematurity and that inhibition of myocardial infarction-associated transcript can downregulate phosphatidylinosital-3-kinase,phosphorylated Akt and vascular endothelial growth factor expression levels and inhibit neovascularization.This study was approved by the Animal Ethics Committee of Shengjing Hospital of China Medical University,China(approval No.2016PS074K)on February 25,2016.