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Updated: Dec 24, 2025

An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
Published on: April 7, 2014
G9a Suppression Alleviates Corneal Neovascularization through Blocking Nox4-Mediated Oxidative Stress
Shanshan Wan1, Wanju Yang1, Yumiao Pan1
1Department of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Background:
G9a, a well-known methyltransferase, plays a vital role in biological processes. However, its role in corneal neovascularization (CoNV) remains unclear. Methods. In vitro and in vivo models were assessed in hypoxia-stimulated angiogenesis and in a mouse model of alkali burn-induced CoNV. Human umbilical vein endothelial cells (HUVECs) were cultured under hypoxic conditions and different reoxygenation times to identify the molecular mechanisms involved in this process.
Results:
In this study, we found that G9a was positively related to corneal alkali burn-induced injury. Inhibition of G9a with BIX 01294 (BIX) alleviated corneal injury, including oxidative stress and neovascularization in vivo models were assessed in hypoxia-stimulated angiogenesis and in a mouse model of alkali burn-induced CoNV. Human umbilical vein endothelial cells (HUVECs) were cultured under hypoxic conditions and different reoxygenation times to identify the molecular mechanisms involved in this process.
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