ArticleInvestigative ophthalmology & visual science2025
ENO2-Regulated Glycolysis in Endothelial Cells Contributes to FGF2-Induced Retinal Neovascularization.
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 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Targeting enolase isoenzyme 2 enables precision glycolysis inhibition in VHL-mutant renal cell carcinoma.Cell death & disease · 2026Article
- Article
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis.Acta pharmacologica Sinica · 2026Article
- An APE1 Redox Inhibitor Attenuates Pathological Retinal Vascularization by Suppressing FGF2 Angiogenic Signaling.Investigative ophthalmology & visual science · 2026Article
- Promotion of angiogenesis in cerebral infarction by Tongqiao Huoxue Decoction through activation of glycolysis.Metabolic brain disease · 2025Article
- PLK2 as a key regulator of glycolysis and immune dysregulation in polycystic ovary syndrome.Frontiers in immunology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Ocular neovascularization is a major cause of blindness. Although fibroblast growth factor-2 (FGF2) has been implicated in the pathophysiology of angiogenesis, the underlying mechanisms remain incompletely understood. The purpose of this study was to investigate the role of FGF2 in retinal neovascularization and elucidate its underlying mechanisms. Methods: The oxygen-induced retinopathy mouse model was used to study the pathogenesis of retinal neovascularization. Immunofluorescence was used to quantify the neovascularization in retina. Data-independent acquisition proteomics were performed to quantify differentially expressed proteins in human retinal microvascular endothelial cells stimulated with FGF2 and associated pathways were analyzed. We carried out qRT-PCR and Western Blot assays to detect the expression of genes at mRNA and protein levels. The angiogenesis abilities of human retinal microvascular endothelial cells were measured by transwell, EdU and tube formation assays. Results: FGF2 was significantly upregulated in retinal tissues of the oxygen-induced retinopathy mouse model and it markedly enhanced tube formation, migration, and proliferation abilities of human retinal microvascular endothelial cells in vitro. The proteomic analysis identified 287 differentially expressed proteins in endothelial cells in response to FGF2 stimulation, characterized by a notable upregulation of the glycolysis pathway, among which we confirmed that the enolase 2 (ENO2) levels were elevated after FGF2 stimulation, and its knockdown resulted in diminished glycolytic activity and impaired angiogenic processes. Furthermore, the use of the ENO2 inhibitor AP-Ⅲ-a4 alleviated angiogenesis in vivo and in vitro. Conclusions: Our findings underscore the pivotal role of ENO2-mediated glycolysis in FGF2-induced angiogenesis, suggesting that ENO2 may serve as a promising therapeutic target for managing pathological neovascularization.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.