ReviewFrontiers in molecular biosciences2024
Pathogenic role of PFKFB3 in endothelial inflammatory diseases.
Review in Frontiers in molecular biosciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed.
- Single-Cell and Machine Learning Analyses Identify a PFKFB3-Centered Regulatory Network and Potential Salidroside Interaction in Coronary Heart Disease.International journal of molecular sciences · 2026Article
- P38γ drives aerobic glycolysis in liver sinusoidal endothelial cells and regulates alcoholic liver disease via the PFKFB3 signaling pathway.Molecular biology reports · 2026Article
- [Research progress on the metabolic regulatory mechanisms of coronary collateral circulation].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Review
- Review
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
- Role of Glycolysis and Nitric Oxide Pathway Crosstalk in Macrophages in Atherosclerosis.Current medicinal chemistry · 2026Review
- PFKFB3 Mediated Glycolytic Reprogramming Drives Vascular Endothelial Injury Under Chronic Intermittent Hypoxia.International journal of biological sciences · 2026Article
- Trained Immunity-Like Memory in Vascular Structural Cells: Metabolic-Epigenetic Reprogramming as a Driving Mechanism of Atherosclerosis and Residual Cardiovascular Risk.Journal of inflammation research · 2026Review
- Metabolic Reprogramming and Cell Interaction in Atherosclerosis: From Molecular Mechanisms to Therapeutic Strategies.Journal of cardiovascular development and disease · 2025Review
- 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The differentiation of vascular endothelial cells and the formation of new blood vessels are inseparable from the energy supply and regulation of metabolism. The budding of blood vessels is a starting point of glycolysis pathway in angiogenesis. Phosphofructokinase-2/fructose 2,6-biophosphatase 3 (PFKFB3), a key rate-limiting enzyme in glycolysis, exhibits strong kinase activity. Inhibition of PFKFB3 can reduce the rate of glycolysis, thereby inhibiting the budding of blood vessels, resulting in inhibition of pathological angiogenesis. In this review, the role of PFKFB3 in the angiogenesis of inflammatory diseases was summarized, and the endothelial inflammatory diseases associated with PFKFB3 were reviewed.
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.