ArticleInvestigative ophthalmology & visual science2025
Inhibition of Retinal Neovascularization by BEZ235: Targeting the Akt/4EBP1/Cyclin D1 Pathway in Endothelial Cells.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The messenger ion: magnesium ion coordinates bone marrow mesenchymal stem cells-mediated osteogenesis, migration, and angiogenesis via the PI3K-AKT-mTOR pathway.Stem cell research & therapy · 2026Article
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Authors and funding
11 authors.
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Abstract
Purpose: To investigate the therapeutic efficacy of BEZ235, a dual PI3K/mTOR inhibitor, in suppressing pathological neovascularization in an oxygen-induced retinopathy (OIR) mouse model and explore the role of cyclin D1 in endothelial cell cycle regulation. Methods: Single-cell RNA sequencing was performed to analyze gene expression and cell-cycle alterations in retinal endothelial cells under normoxic and OIR conditions. The effects of BEZ235 on human umbilical vein endothelial cells (HUVECs) and human retinal microvascular endothelial cells (HRMECs) were evaluated by assessing cell viability, cell-cycle progression, proliferation, migration, and tube formation. In the OIR mouse model, retinal neovascularization was evaluated by retinal flatmount immunofluorescence staining, hematoxylin and eosin (H&E) staining, quantitative reverse-transcription polymerase chain reaction (RT-qPCR), and western blot analyses. The in vivo toxicity of BEZ235 was evaluated by electroretinography (ERG) and histological examination of the heart, liver, spleen, lungs, and kidneys. Results: In vitro, BEZ235 significantly inhibited cell cycle progression by downregulating cyclin D1 at both mRNA and protein levels, inducing G0/G1 phase arrest. This led to significant reductions in cell viability, proliferation, migration, and tube formation. In the OIR model, BEZ235 substantially decreased neovascularization and improved vascular organization. BEZ235 mediates its effects by inhibiting the PI3K/Akt/mTOR pathway, reducing Akt and 4E-binding protein 1 (4EBP1) phosphorylation levels, thus downregulating cyclin D1 expression. ERG and histological examination suggested that BEZ235 did not induce evident retinal or systemic toxicity at the dosage used to inhibit retinal neovascularization. Conclusions: BEZ235 effectively inhibits retinal neovascularization by downregulating cyclin D1 via 4EBP1 phosphorylation inhibition, highlighting its potential as a promising therapeutic agent for retinal neovascularization diseases.
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