Related Experiment Video

Updated: Feb 24, 2026

An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
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An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse

Published on: April 7, 2014

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YBX1 Modulated Corneal Neovascularization Induced by Alkali Burn via m5C-Dependent Regulation of the

Zixian Yang1, Yulin Yan1, Qian Deng1

  • 1Department of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.

Investigative Ophthalmology & Visual Science
|February 23, 2026
PubMed
Abstract

Insights

YBX1 drives corneal neovascularization (CoNV) by stabilizing specific mRNAs. Inhibiting YBX1 with Soyasaponin II (SII) offers a promising therapeutic strategy for treating CoNV.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Epigenetics

Background:

  • Corneal neovascularization (CoNV) poses a significant challenge in ophthalmology.
  • The role of epitranscriptomic modifications, like N5-methylcytosine (m5C), in CoNV is not fully understood.
  • RNA-binding proteins are increasingly recognized for their roles in regulating gene expression.

Purpose of the Study:

  • To investigate the function and mechanism of the RNA-binding protein YBX1 in corneal neovascularization (CoNV) induced by alkali burn (AB).
  • To explore the role of m5C modification in YBX1-mediated CoNV.
  • To evaluate the therapeutic potential of a YBX1 inhibitor for CoNV.

Main Methods:

  • Established an alkali burn-induced CoNV mouse model and used hypoxia/reoxygenation (H/R) in human umbilical vein endothelial cells (HUVECs) in vitro.
  • Employed multi-omics approaches including transcriptome sequencing, RNA immunoprecipitation sequencing, and m5C methylated RNA immunoprecipitation sequencing.
  • Conducted functional assays for angiogenesis, apoptosis, and reactive oxygen species (ROS), and evaluated the in vivo therapeutic effect of Soyasaponin II (SII).

Main Results:

  • YBX1 expression was upregulated in CoNV models.
  • YBX1 knockdown inhibited HUVEC migration, tube formation, and ROS production, while promoting apoptosis, effects rescued by HIF-1α.
  • YBX1 enhances STAT3 and VEGFA mRNA stability via m5C modification, activating the JAK1/STAT3 pathway.

Conclusions:

  • YBX1 drives CoNV through an epitranscriptomic mechanism involving m5C-modified STAT3 and VEGFA mRNA stabilization, activating the JAK1/STAT3/HIF-1α axis.
  • Inhibition of YBX1 using Soyasaponin II (SII) effectively counteracts this pathway.
  • YBX1 is identified as a potential therapeutic target for sight-threatening CoNV.

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