ArticleFrontiers in cell and developmental biology2020
Inhibition of PFKFB3 Hampers the Progression of Atherosclerosis and Promotes Plaque Stability.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 65 citations in OpenAlex.
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- 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
- Research Progress on Downstream Mechanisms of Glucose Metabolic Reprogramming and Its Role in the Occurrence and Progression of Type 2 Diabetes Mellitus.Biomedicines · 2026Review
- RNA-Based Biomarkers for Diagnostic Discrimination of Ischemic and Hemorrhagic Stroke: A Systematic Review.Journal of clinical medicine · 2026Review
- Glucose Metabolic Enzyme PFKFB3 in Cardiopulmonary Vascular Health and Disease.Circulation research · 2026Review
- Inhibition of PFKFB3 in macrophages ameliorates intestinal inflammation by modulating gut microbiota in DSS-induced colitis.mSystems · 2026Article
- Immune checkpoint inhibitor-induced cardiotoxicity: from immune mechanisms to clinical surveillance and targeted therapies.Frontiers in cardiovascular medicine · 2026Review
- Role of Glycolysis and Nitric Oxide Pathway Crosstalk in Macrophages in Atherosclerosis.Current medicinal chemistry · 2026Review
- Endothelial Metabolic Reprogramming Links Diabetes to Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Vascular smooth muscle cell metabolic reprogramming and phenotypic remodeling in atherosclerosis.Cell death discovery · 2025Review
- Reprogrammed glucose metabolism in vascular smooth muscle cells and its implications for vascular diseases.Pharmacological research · 2025Review
- Role of COUP‑TFII in cardiovascular diseases and colorectal cancer: Insights into the molecular mechanisms and clinical relevance (Review).Molecular medicine reports · 2025Review
- Impacts of aging and fluid shear stress on vascular endothelial metabolism and atherosclerosis development.Journal of biomedical science · 2025Review
- Adiponectin mediated metabolic and sphingolipid alterations in preventing endothelial dysfunction.Molecular and cellular biochemistry · 2025Article
- Fuelling aortic stenosis: the integral role of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3-mediated glycolysis in Lp(a)-induced valve inflammation.European heart journal open · 2025Article
- A dual-targeting bio-liposomes nanodrug repair endothelial cell dysfunction and restore macrophage cholesterol flow homeostasis to treat early atherosclerosis.Journal of nanobiotechnology · 2025Article
- Macrophage HM13/SPP Enhances Foamy Macrophage Formation and Atherogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Metabolic reprogramming and interventions in angiogenesis.Journal of advanced research · 2025Review
- ICI-induced cardiovascular toxicity: mechanisms and immune reprogramming therapeutic strategies.Frontiers in immunology · 2025Review
- Active LXR signaling, coupled with elevated mitochondrial and glycolytic metabolism contributes to GM-CSF-induced trained immunity.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims6-phosphofructo-2-kinase/fructose-2,6-biphosphatase (PFKFB)3-mediated glycolysis is pivotal in driving macrophage- and endothelial cell activation and thereby inflammation. Once activated, these cells play a crucial role in the progression of atherosclerosis. Here, we analyzed the expression of PFKFB3 in human atherosclerotic lesions and investigated the therapeutic potential of pharmacological inhibition of PFKFB3 in experimental atherosclerosis by using the glycolytic inhibitor PFK158. METHODS AND
resultsPFKFB3 expression was higher in vulnerable human atheromatous carotid plaques when compared to stable fibrous plaques and predominantly expressed in plaque macrophages and endothelial cells. Analysis of advanced plaques of human coronary arteries revealed a positive correlation of PFKFB3 expression with necrotic core area. To further investigate the role of PFKFB3 in atherosclerotic disease progression, we treated 6-8 weeks old male
conclusionHigh PFKFB3 expression is associated with vulnerable atheromatous human carotid and coronary plaques. In mice, high PFKFB3 expression is also associated with a vulnerable plaque phenotype, whereas inhibition of PFKFB3 activity leads to plaque stabilization. This data implies that inhibition of inducible glycolysis may reduce inflammation, which has the ability to subsequently attenuate atherogenesis.
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