ArticleMolecular biology reports2021
The effects of hyperuricemia on endothelial cells are mediated via GLUT9 and the JAK2/STAT3 pathway.
Article in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Maternal hyperuricemia and adverse maternal-fetal outcomes: a systematic review and meta-analysis of observational studies.Frontiers in medicine · 2026Pooled it
- SLC2A9-Mediated Uric Acid Homeostasis Modulates Apoptosis in TNBC.Breast cancer (Dove Medical Press) · 2026Article
- From arthritis to erectile dysfunction: potential pathophysiological mechanisms and multidisciplinary integrated management.Frontiers in cell and developmental biology · 2026Review
- Therapeutic potential of traditional Chinese medicine for hyperuricemia: mechanistic insights and clinical prospects.Frontiers in pharmacology · 2026Review
- Uric acid and ammonia play synergistic roles in the loss of blood-brain barrier integrity in the context of hepatic encephalopathy.Fluids and barriers of the CNS · 2025Article
- Hyperuricemia in Chronic Kidney Disease: Emerging Pathophysiology and a Novel Therapeutic Strategy.International journal of molecular sciences · 2025Review
- Epigenetic isoforms (DNMT3A/3B and HDAC3/7) potential predictors of endothelial dysfunction and subclinical atherosclerosis.Molecular biology reports · 2025Review
- Alteration in epigenetic profile in subclinical atherosclerosis and in high uric acid.Scientific reports · 2025Article
- Isoliquiritigenin Promotes the Repair of High Uric Acid-Induced Vascular Injuries.Smart medicine · 2025Article
- Associations between serum uric acid levels and hypotension after general anesthesia induction in hypertensive patients.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Article
- Effects of allopurinol and febuxostat on uric acid transport and transporter expression in human umbilical vein endothelial cells.PloS one · 2024Article
- TCM and related active compounds in the treatment of gout: the regulation of signaling pathway and urate transporter.Frontiers in pharmacology · 2023Review
- Wuling San Based on Network Pharmacology and in vivo Evidence Against Hyperuricemia via Improving Oxidative Stress and Inhibiting Inflammation.Drug design, development and therapy · 2023Article
- Apigenin Ameliorates Hyperuricemia and Renal Injury through Regulation of Uric Acid Metabolism and JAK2/STAT3 Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2022Article
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6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundUric acid (UA) transporters mediate the uptake and outflow of UA, and are greatly involved in the control of UA concentrations. Glucose transporter 9 (GLUT9), one of the UA transporters, has been confirmed to be expressed in human umbilical vein endothelial cells (HUVECs). This study aimed to characterize GLUT9's effect on intracellular UA accumulation in HUVECs in a high-UA environment and to explore the mechanism of cellular dysfunction. METHODS AND
resultsHUVECs were treated with UA to establish a model of cellular dysfunction. Then, UA uptake, GLUT9 expression and endothelial nitric oxide synthase (eNOS) and reactive oxygen species (ROS) amounts were measured. UA uptake was concentration- and time-dependent, and UA treatment significantly reduced nitric oxide (NO) levels and eNOS activity. UA also upregulated pro-inflammatory molecules and GLUT9, and increased intracellular ROS amounts in HUVECs. GLUT9 knockdown reduced UA uptake and ROS content, but antioxidant treatment did not reduce GLUT9 expression. To assess the function of JAK2/STAT3 signaling, HUVECs were treated with UA, and the phosphorylation levels of JAK2, STAT3, IL-6 and SOCS3 were increased by a high concentration of UA. In addition, GLUT9 knockdown reduced the phosphorylation of JAK2/STAT3 intermediates and increased p-eNOS amounts.
conclusionsGLUT9 mediated the effects of high UA levels on HUVECs by increasing the cellular uptake of UA, activating JAK2/STAT3 signaling, and reduced the production of active eNOS and NO in HUVECs.
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