Evidence map›Paper›PMID 41729046›Full record

ArticleInvestigative ophthalmology & visual science2026

YBX1 Modulated Corneal Neovascularization Induced by Alkali Burn via m5C-Dependent Regulation of the STAT3/HIF-1α/VEGFA Axis.

Zixian Yang, Yulin Yan, Qian Deng, Yuelan Gao, Jiewen Mao, Lan Ke, Shanshan Wan, Yanning Yang

Abstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Zixian YangDepartment of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Yulin YanDepartment of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Qian DengDepartment of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Yuelan GaoDepartment of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Jiewen MaoDepartment of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Lan KeDepartment of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Shanshan WanDepartment of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Yanning YangDepartment of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Effective management of corneal neovascularization (CoNV) remains challenging, and the role of epitranscriptomic regulation, particularly N5-methylcytosine (m5C) modification, in this process remain incompletely defined. This study investigated the function and mechanism of the RNA-binding protein YBX1 in CoNV following alkali burn (AB). Methods: An AB-induced CoNV model was generated using C57BL/6 mice. In vitro, human umbilical vein endothelial cells (HUVECs) underwent hypoxia/reoxygenation (H/R). Multi-omics approaches including transcriptome sequencing, RNA immunoprecipitation sequencing, and m5C methylated RNA immunoprecipitation sequencing were used to identify YBX1 targets and their modification status. Functional assays assessed angiogenesis, apoptosis, and reactive oxygen species (ROS). The therapeutic potential of the YBX1 inhibitor Soyasaponin II (SII) was evaluated in vivo. Results: YBX1 was upregulated following AB and H/R. YBX1 knockdown suppressed HUVEC migration, tube formation, and ROS production, while promoting apoptosis; these effects were rescued by HIF-1α overexpression. Mechanistically, YBX1 activated the JAK1/STAT3 pathway and recognizes m5C-modified sequences on STAT3 and VEGFA mRNAs, enhancing their stability. In vivo, subconjunctival injection of SII attenuated CoNV, reduced inflammation, and modulated macrophage polarization. Conclusions: Our study unveils a novel epitranscriptomic mechanism in which YBX1 drives CoNV by regulating the stability of m5C-modified STAT3 and VEGFA mRNAs, thereby activating the JAK1/STAT3/HIF-1α axis. Inhibition of YBX1 with SII effectively counteracts this pathway, highlighting YBX1 as an attractive candidate for intervention against sight-threatening CoNV.

Indexed as

Burns, ChemicalCorneal NeovascularizationEye BurnsGene Expression RegulationHypoxia-Inducible Factor 1, alpha SubunitSTAT3 Transcription FactorVascular Endothelial Growth Factor AY-Box-Binding Protein 1AnimalsApoptosisBlotting, WesternCells, CulturedDisease Models, AnimalHumansHuman Umbilical Vein Endothelial CellsMaleHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitReactive Oxygen SpeciesStat3 protein, mouseSTAT3 Transcription FactorVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseY-Box-Binding Protein 1YBX1 protein, human

Identifiers

PMID41729046
PMCPMC12934531

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.