ArticleHypertension (Dallas, Tex. : 1979)2023
Type 1 Diabetes Impairs Endothelium-Dependent Relaxation Via Increasing Endothelial Cell Glycolysis Through Advanced Glycation End Products, PFKFB3, and Nox1-Mediated Mechanisms.
Article in Hypertension (Dallas, Tex. : 1979), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Endothelial Drp1 integrates VEGF-induced redox signaling with glycolysis through cysteine oxidation to drive angiogenesis.Nature communications · 2026Article
- Novel AI-Driven Precision Strategies in Diabetic Wound Healing: Immunomodulation and Advances in Smart Composite Nanocarriers.Pharmaceutics · 2026Review
- Glycation metabolites predict incident age-related comorbidities and mortality in older people with HIV.GeroScience · 2026Article
- Glycolytic reprogramming and immune responses in macrophages: a crosstalk driven by bacterial infection.Frontiers in immunology · 2026Review
- Diabetes Status Modifies the Association Between Carotid Plaque Burden and Retinal Microvascular Parameters.International journal of medical sciences · 2026Article
- Endothelial Metabolic Reprogramming Links Diabetes to Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Advanced glycation end products induce inflammaging in periodontal ligament fibroblasts through RAGE/AKT/mTOR/glycolysis pathway.Acta odontologica Scandinavica · 2025Article
- Are You a Friend or an Enemy? The Dual Action of Methylglyoxal on Brain Microvascular Endothelial Cells.International journal of molecular sciences · 2025Article
- PFKFB3 Connects Glycolytic Metabolism with Endothelial Dysfunction in Human and Rodent Obesity.Antioxidants (Basel, Switzerland) · 2025Article
- Research Progress on Glycolysis in the Pathogenesis of Asthma.Journal of asthma and allergy · 2025Review
- Identification of key genes of diabetic cardiomyopathy in hiPSCs-CMs based on bioinformatics analysis.Molecular and cellular biochemistry · 2024Article
- Histidine containing dipeptides protect epithelial and endothelial cell barriers from methylglyoxal induced injury.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundType 1 diabetes (T1D) is a major cause of endothelial dysfunction. Although cellular bioenergetics has been identified as a new regulator of vascular function, whether glycolysis, the primary bioenergetic pathway in endothelial cells (EC), regulates vascular tone and contributes to impaired endothelium-dependent relaxation (EDR) in T1D remains unknown.
methodsExperiments were conducted in Akita mice with intact or selective deficiency in EC PFKFB3 (6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3), the main regulator of glycolysis. Seahorse analyzer and myography were employed to measure glycolysis and mitochondrial respiration, and EDR, respectively, in aortic explants. EC PFKFB3 (Ad-PFKFB3) and glycolysis (Ad-GlycoHi) were increased in situ via adenoviral transduction.
resultsT1D increased EC glycolysis and elevated EC expression of PFKFB3 and NADPH oxidase Nox1 (NADPH oxidase homolog 1). Functionally, pharmacological and genetic inhibition of PFKFB3 restored EDR in T1D, while in situ aorta EC transduction with Ad-PFKFB3 or Ad-GlycoHi reproduced the impaired EDR associated with T1D. Nox1 inhibition restored EDR in aortic rings from Akita mice, as well as in Ad-PFKFB3-transduced aorta EC and lactate-treated wild-type aortas. T1D increased the expression of the advanced glycation end product precursor methylglyoxal in the aortas. Exposure of the aortas to methylglyoxal impaired EDR, which was prevented by PFKFB3 inhibition. T1D and exposure to methylglyoxal increased EC expression of HIF1α (hypoxia-inducible factor 1α), whose inhibition blunted methylglyoxal-mediated EC PFKFB3 upregulation.
conclusionsEC bioenergetics, namely glycolysis, is a new regulator of vasomotion and excess glycolysis, a novel mechanism of endothelial dysfunction in T1D. We introduce excess methylglyoxal, HIF1α, and PFKFB3 as major effectors in T1D-mediated increased EC glycolysis.
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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 Socratic graph.