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Updated: Dec 25, 2025

Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
CCAAT/Enhancer-Binding Protein β Mediates Oxygen-Induced Retinal Neovascularization via Retinal Vascular Damage and
Tingting Li1, Xuan Cai1, Xiangning Wang1
1Department of Ophthalmology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, China.
Objective:
To evaluate the role of CCAAT/enhancer-binding protein β (C/EBP β (C/EBP.
Methods:
Rats with OIR were exposed to alternating hypoxic and hyperopic conditions for 14 days. Then, the rats with OIR were assigned randomly to groups that received intravitreal injections of either shRNA lentiviral particles targeting C/EBP β (C/EBP β (C/EBP β (C/EBP β (C/EBP β (C/EBP β (C/EBP.
Results:
In OIR rats, the expression levels of C/EBP β (C/EBP P < 0.01). The p-C/EBP β (C/EBP β (C/EBP β (C/EBP β (C/EBP β (C/EBP P < 0.01). The p-C/EBP β (C/EBP β (C/EBP β (C/EBP P < 0.01). The p-C/EBP.
Conclusions:
C/EBP β shRNA inhibits RNV in OIR. A potential mechanism may be that the activity of C/EBP β increases with its overexpression, which in turn aggravates the amount of the retinal vascular damage and promotes transcription of VEGF. C/EBP β might be a new therapeutic target for preventing RNV.β (C/EBP β (C/EBP β (C/EBP.
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