ArticleDiabetology & metabolic syndrome2015
High glucose induces and activates Toll-like receptor 4 in endothelial cells of diabetic retinopathy.
Article in Diabetology & metabolic syndrome, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 74 citations in OpenAlex.
- Impact of Glycemic Trajectory and Variability on Ischemic Stroke Prognosis and Exploration of Its Mechanisms: A Comprehensive Review.Healthcare (Basel, Switzerland) · 2026Review
- When glycobiology meets inflammasome activation: Insights and implications.Journal of advanced research · 2026Review
- Systems biology and microbiome innovations for personalized diabetic retinopathy management.NPJ systems biology and applications · 2025Review
- Article
- Impacts of sulfate polysaccharide JCS1S2 on retinal neovascularization in oxygen-induced retinopathy rats.Frontiers in pharmacology · 2025Article
- Drugless peptide-based nanohybrids alleviate diabetic retinopathy by suppressing microglial activation and endothelial inflammation.Theranostics · 2025Article
- Preoperative hemoglobin A1c is associated with postoperative bleeding after vitrectomy for vitreous hemorrhage in patients with diabetic retinopathy.Endocrine journal · 2024Article
- The Functions of SARS-CoV-2 Receptors in Diabetes-Related Severe COVID-19.International journal of molecular sciences · 2024Review
- Ischemic stroke and diabetes: a TLR4-mediated neuroinflammatory perspective.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Hyperglycaemia Aggravates Oxidised Low-Density Lipoprotein-Induced Schwann Cell Death via Hyperactivation of Toll-like Receptor 4.Neurology international · 2024Article
- The contribution of pattern recognition receptor signalling in the development of age related macular degeneration: the role of toll-like-receptors and the NLRP3-inflammasome.Journal of neuroinflammation · 2024Review
- Lipotoxicity and immunometabolism in ischemic acute kidney injury: current perspectives and future directions.Frontiers in pharmacology · 2024Review
- Neurovascular Cell Death and Therapeutic Strategies for Diabetic Retinopathy.International journal of molecular sciences · 2023Review
- Pathomorphological Manifestations and the Course of the Cervical Cancer Disease Determined by Variations in theDiagnostics (Basel, Switzerland) · 2023Article
- Suppressing Inflammation for the Treatment of Diabetic Retinopathy and Age-Related Macular Degeneration: Dazdotuftide as a Potential New Multitarget Therapeutic Candidate.Biomedicines · 2023Review
- Endothelial Dysfunction in Patients Undergoing Cardiac Surgery: A Narrative Review and Clinical Implications.Journal of cardiovascular development and disease · 2023Review
- RAGE-TLR4 Crosstalk Is the Key Mechanism by Which High Glucose Enhances the Lipopolysaccharide-Induced Inflammatory Response in Primary Bovine Alveolar Macrophages.International journal of molecular sciences · 2023Article
- Antimicrobial Peptide LCN2 Inhibited UropathogenicInternational journal of molecular sciences · 2022Article
- Retinal Transcriptome and Cellular Landscape in Relation to the Progression of Diabetic Retinopathy.Investigative ophthalmology & visual science · 2022Article
- High glucose enhances lipopolysaccharide-induced inflammation in cultured BV2 microglial cell line.Immunity, inflammation and disease · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHyperglycemia-induced inflammation causes the dysfunction of blood vessels, and Toll-like receptor 4 (TLR4) plays a key role in inflammation-induced angiogenesis. However, the impact of TLR4 on the pathogenesis of diabetic retinopathy (DR) is poorly understood. In this study, we examined the expression of TLR4 in retinal vascular endothelial cells of patients with DR and diabetic mice, and explored the role of TLR4 in mediating inflammatory responses by human microvascular endothelial cells (HMEC-1) under high-glucose condition.
methodsThe expression of TLR4 in retinal vascular endothelial cells of patients with proliferative diabetic retinopathy and diabetic mice induced by streptozotocin was examined using immunofluorescence. HMEC-1 cells were cultured and the expression of TLR4, MyD88 and Interleukin-1β (IL-1β) was examined under high-glucose condition. Endothelial cells with TLR4 silencing and antagonist of TLR4 as well as endothelial cells from TLR4 deficient mice were used to study the effect of activated TLR4 on inflammation induced by high-glucose treatment.
resultsWe observed that TLR4 was detected in CD31-labled human retinal vascular endothelia and its expression was markedly increased in fibrovascular membranes from DR patients and in retinal vascular endothelial cells of diabetic mice. The expression of TLR4, MyD88 and IL-1β was enhanced by high glucose in cultured HMEC-1 and the expression of TLR4 and IL-1β was inhibited by TLR4 siRNA knock-down and TLR4 antagonist. The expression of IL-1β by endothelial cells from TLR4 deficient mice under high glucose condition was decreased.
conclusionsOur results revealed that hyperglycemia induced overexpression and activation of TLR4 in endothelial cells. This effect may lead to inflammatory responses contribute to the pathogenesis of diabetic retinopathy.
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