ArticleAmerican journal of physiology. Renal physiology2012
Interaction between uric acid and HMGB1 translocation and release from endothelial cells.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 77 citations in OpenAlex.
- Trial
- Preclinical evaluation of sodium copper chlorophyllin: safety, pharmacokinetics, and therapeutic potential in breast cancer chemotherapy and cyclophosphamide-induced bladder toxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Association between the uric acid-to-HDL-cholesterol ratio (UHR) and the risk of cardiovascular disease and dyslipidemia: a population-based study.Lipids in health and disease · 2025Article
- Kidney function in newly diagnosed myeloma patients: factors associated with kidney impairment and recovery.BMC nephrology · 2024Article
- Hyperuricemia and its related diseases: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024Review
- Progress of uric acid in cardiovascular disease.Cardiovascular endocrinology & metabolism · 2024Review
- Machine learning-based comparison of factors influencing estimated glomerular filtration rate in Chinese women with or without non-alcoholic fatty liver.World journal of clinical cases · 2024Article
- Article
- Effect of Intestinal Flora on Hyperuricemia-Induced Chronic Kidney Injury in Type 2 Diabetic Patients and the Therapeutic Mechanism of New Anti-Diabetic Prescription Medications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Review
- Modification of mesenchymal stem cells by HMGB1 promotes the activity of Cav3.2 T-type calcium channel via PKA/β-catenin/γ-cystathionase pathway.Stem cell research & therapy · 2022Article
- Inhibition of inflammatory liver injury by the HMGB1-A box through HMGB1/TLR-4/NF-κB signaling in an acute liver failure mouse model.Frontiers in pharmacology · 2022Article
- Interleukin-22 in Renal Protection and Its Pathological Role in Kidney Diseases.Frontiers in immunology · 2022Review
- Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2021Review
- The Key Role of Uric Acid in Oxidative Stress, Inflammation, Fibrosis, Apoptosis, and Immunity in the Pathogenesis of Atrial Fibrillation.Frontiers in cardiovascular medicine · 2021Review
- Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment.BioMed research international · 2021Review
- Endothelial dysfunction in neuroprogressive disorders-causes and suggested treatments.BMC medicine · 2020Review
- Serum Uric Acid and Mortality Risk Among Hemodialysis Patients.Kidney international reports · 2020Article
- Risk factors for renal failure and short-term prognosis in patients with spontaneous intracerebral haemorrhage complicated by acute kidney injury.BMC nephrology · 2020Article
- Research Advances in the Mechanisms of Hyperuricemia-Induced Renal Injury.BioMed research international · 2020Review
- Evolving spectrum of diabetic nephropathy.World journal of diabetes · 2019Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
We aimed to investigate the potential relationship between alarmins [acting via Toll-like receptor-4 (TLR4)], uric acid (UA), and high-mobility group box-1 protein (HMGB1) during acute kidney injury. UA, which is significantly increased in the circulation following renal ischemia-reperfusion injury (IRI), was used both in vitro and in vivo as an early response-signaling molecule to determine its ability to induce the secretion of HMGB1 from endothelial cells. Treatment of human umbilical vein endothelial cells (HUVEC) with UA resulted in increased HMGB1 mRNA expression, acetylation of nuclear HMGB1, and its subsequent nuclear-cytoplasmic translocation and release into the circulation, as determined by Western blotting and immunofluorescence. Treatment of HUVEC with UA and a calcium mobilization inhibitor (TMB-8) or a MEK/Erk pathway inhibitor (U0126) prevented translocation of HMGB1 from the nucleus, resulting in reduced cytoplasmic and circulating levels of HMGB1. Once released, HMGB1 in autocrine fashion promoted further HMGB1 release while also stimulating NF-κB activity and increased angiopoietin-2 expression and protein release. Transfection of HUVEC with TLR4 small interfering (si) RNA reduced HMGB1 levels during UA and HMGB1 treatment. In summary, UA after IRI mediates the acetylation and release of HMGB1 from endothelial cells by mechanisms that involve calcium mobilization, the MEK/Erk pathway, and activation of TLR4. Once released, HMGB1 promotes its own further cellular release while acting as an autocrine and paracrine to activate both proinflammatory and proreparative mediators.
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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.