Evidence map›Paper›PMID 42897656›Full record

ArticleBiology direct2026

ZRANB1-mediated EZH2 stabilization drives S100B/S100A4 transcriptional activation and corneal neovascularization in alkali burns.

Fangyuan Liu, Ying Xiao, Yeping Huang, Yang Liu, Zhiyou Peng, Yulin Wang

Abstract read
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In one paragraph

Article in Biology direct, 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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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Fangyuan Liu *Department of Ophthalmology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwaizheng Street, Nanchang, Jiangxi, 330006, China.
Ying Xiao *Department of Ophthalmology, First Affiliated Hospital of Jinggangshan University, Ji'an, Jiangxi, China.
Yeping HuangDepartment of Ophthalmology, The People's Hospital of Wanzai County, Yichun, Jiangxi, China.
Yang LiuDepartment of Ophthalmology, Duchang County People's Hospital in Jiujiang City, Jiujiang, Jiangxi, China.
Zhiyou PengDepartment of Ophthalmology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwaizheng Street, Nanchang, Jiangxi, 330006, China.
Yulin WangDepartment of Ophthalmology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwaizheng Street, Nanchang, Jiangxi, 330006, China. Ndyfy02107@ncu.edu.cn.

Funding

Project of Regional Science Foundation of National Natural Science Foundation 82060174Science and Technology Plan of Jiangxi Provincial Health Commission 202310207
6 · The paper itself

Abstract

Alkali burn is one of the main causes of corneal injury. Corneal neovascularization caused by alkali burns aggravates corneal damage, resulting in aberrant vascular proliferation and consequent visual impairment. The present study investigated the role of enhancer of zeste homolog 2 (EZH2) in alkali burn‑induced corneal neovascularization. Through integrated bioinformatics and experimental approaches, we identified S100B, S100A4 and PI3K/AKT pathway activation as key drivers of alkali-induced corneal injury. In corneal alkali burn mice, knockdown of S100B or S100A4 attenuated corneal neovascularization and suppressed PI3K/AKT/FoxO3a pathway. EZH2 was upregulated in alkali-burn models and transcriptionally activated S100B and S100A4 via direct promoter binding. The deubiquitinase ZRANB1 was identified to stabilize EZH2 protein through deubiquitination, thereby amplifying its transcriptional activity. In alkali-injured human corneal epithelial cells, EZH2 overexpression enhanced cell viability, angiogenic capacity, migration and invasion ability, which was reversed by S100B or S100A4 knockdown. In vivo, EZH2 overexpression exacerbated PI3K/AKT/FoxO3a pathway activation and corneal neovascularization via regulating S100B or S100A4. Collectively, this study demonstrated that ZRANB1-mediated stabilization of EZH2 drove pathological corneal angiogenesis in corneal alkali burns by activating S100B/S100A4-PI3K/AKT/FoxO3a axis. These findings provided novel therapeutic targets for corneal alkali burns.

Indexed as

Burns, ChemicalCorneal NeovascularizationEnhancer of Zeste Homolog 2 ProteinEye BurnsRNA-Binding ProteinsS100 Calcium-Binding Protein A4S100 Calcium Binding Protein beta SubunitAlkaliesAnimalsForkhead Box Protein O3HumansMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesTranscriptional ActivationAlkaliesEnhancer of Zeste Homolog 2 ProteinEzh2 protein, mouseForkhead Box Protein O3Phosphatidylinositol 3-KinasesRNA-Binding ProteinsS100A4 protein, humanS100 Calcium-Binding Protein A4S100 Calcium Binding Protein beta SubunitCorneal alkali burnCorneal neovascularizationDeubiquitinationEZH2PI3K/AKT/FoxO3aS100B/S100A4

Identifiers

PMID42897656
PMCPMC13679132

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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.