ArticleArteriosclerosis, thrombosis, and vascular biology2017
Glucose Transporter 3 Potentiates Degranulation and Is Required for Platelet Activation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- The Glucose Transporter GLUT3 Controls Regulatory T Cell Function.European journal of immunology · 2026Article
- Systemic metabolic dysfunction drives platelet-mediated inflammation, fibrogenesis, and hepatocarcinogenesis in metabolic dysfunction-associated steatotic liver disease.Clinical and molecular hepatology · 2026Review
- Platelet mitochondria dysfunction in diabetes mellitus: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Mitochondrial Calcium Uniporter Regulates ITAM-Dependent Platelet Activation.Circulation research · 2025Article
- Article
- Platelets and diseases: signal transduction and advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Shared genes and relevant potential molecular linkages between COVID-19 and chronic thromboembolic pulmonary hypertension (CTEPH).Journal of thrombosis and thrombolysis · 2025Article
- Mitofusin-2 Regulates Platelet Mitochondria and Function.Circulation research · 2024Article
- Novel 4th-generation phytase improves broiler growth performance and reduces woody breast severity through modulation of muscle glucose uptake and metabolism.Frontiers in physiology · 2024Article
- Review
- Preeclampsia: Platelet procoagulant membrane dynamics and critical biomarkers.Research and practice in thrombosis and haemostasis · 2023Article
- The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming.Cell metabolism · 2022Article
- Rodent models of pulmonary embolism and chronic thromboembolic pulmonary hypertension.Heliyon · 2022Review
- Identification of molecular mechanism and key biomarkers in membranous nephropathy by bioinformatics analysis.American journal of translational research · 2022Article
- Analysis of glucose metabolism byScientific reports · 2021Article
- It takes a village: lessons from collaborative science.The Journal of clinical investigation · 2021Article
- A Multivariate Metabolomics Method for Estimating Platelet Mitochondrial Oxygen Consumption Rates in Patients with Sepsis.Metabolites · 2020Article
- Glucose Metabolism Is Required for Platelet Hyperactivation in a Murine Model of Type 1 Diabetes.Diabetes · 2019Article
- Nox2 NADPH oxidase is dispensable for platelet activation or arterial thrombosis in mice.Blood advances · 2019Article
- Aerobic glycolysis fuels platelet activation: small-molecule modulators of platelet metabolism as anti-thrombotic agents.Haematologica · 2019Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveOn activation, platelets increase glucose uptake, glycolysis, and glucose oxidation and consume stored glycogen. This correlation between glucose metabolism and platelet function is not well understood and even less is known about the role of glucose metabolism on platelet function in vivo. For glucose to enter a cell, it must be transported through glucose transporters. Here we evaluate the contribution of GLUT3 (glucose transporter 3) to platelet function to better understand glucose metabolism in platelets. APPROACH AND
resultsPlatelet-specific knockout of GLUT3 was generated by crossing mice harboring GLUT3 floxed allele to a PF4 (platelet factor 4)-driven Cre recombinase. In platelets, GLUT3 is localized primarily on α-granule membranes and under basal conditions facilitates glucose uptake into α-granules to be used for glycolysis. After activation, platelets degranulate and GLUT3 translocates to the plasma membrane, which is responsible for activation-mediated increased glucose uptake. In vivo, loss of GLUT3 in platelets increased survival in a collagen/epinephrine model of pulmonary embolism, and in a K/BxN model of autoimmune inflammatory disease, platelet-specific GLUT3 knockout mice display decreased disease progression. Mechanistically, loss of GLUT3 decreased platelet degranulation, spreading, and clot retraction. Decreased α-granule degranulation is due in part to an impaired ability of GLUT3 to potentiate exocytosis.
conclusionsGLUT3-mediated glucose utilization and glycogenolysis in platelets promotes α-granule release, platelet activation, and postactivation functions.
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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 OpenQuestion graph.