ArticleGrowth factors (Chur, Switzerland)2018
HMGB1 inhibits insulin signalling through TLR4 and RAGE in human retinal endothelial cells.
Article in Growth factors (Chur, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- Effects of High-Dextrose Intake on the Structural and Functional Properties of the Small Intestine in Young-Maturing and Middle-Aged Rats.International journal of molecular sciences · 2026Article
- The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026Review
- Investigating the protective effect of zinc supplementation on streptozotocin-induced pancreatic beta-cell damage via the HMGB1/TLR2/MAPK pathway.Iranian journal of basic medical sciences · 2026Article
- Role of exchange proteins directly activated by cAMP signaling in vascular remodeling.Pharmacological reviews · 2025Review
- Restoring glucose balance: Conditional HMGB1 knockdown mitigates hyperglycemia in a Streptozotocin induced mouse model.Heliyon · 2024Article
- Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.Endocrine reviews · 2023Review
- Effects of Diabetes Mellitus-Related Dysglycemia on the Functions of Blood-Brain Barrier and the Risk of Dementia.International journal of molecular sciences · 2023Review
- Regulatory mechanisms of HMGB1 and its receptors in polycystic ovary syndrome-driven gravid uterine inflammation.The FEBS journal · 2023Article
- Toll-Like Receptor Signalling Pathways and the Pathogenesis of Retinal Diseases.Frontiers in ophthalmology · 2022Review
- Article
- Loss of TLR4 in endothelial cells but not Müller cells protects the diabetic retina.Experimental eye research · 2021Article
- Mechanism of HMGB1-RAGE in Kawasaki disease with coronary artery injury.European journal of medical research · 2020Article
- Downregulation of Lysosomal Acid Ceramidase Mediates HMGB1-Induced Migration and Proliferation of Mouse Coronary Arterial Myocytes.Frontiers in cell and developmental biology · 2020Article
- High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives.International journal of molecular sciences · 2019Review
- The role of high mobility group box-1 on the development of diabetes complications: A plausible pharmacological target.Diabetes & vascular disease researchReview
- Effects of Glycyrrhizin Treatment on Diabetic Cornea.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and TherapeuticsArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In the past decade, the role of inflammation has been shown in diabetes and its complications. Little is available on high mobility group box 1 (HMGB1) actions on the proteins involved in insulin signal transduction, which may be altered to result in insulin resistance in the retina. Retinal endothelial cells (REC) were grown in normal or high glucose and treated with recombinant human HMGB1, an Epac1 agonist, or both. Additional cells were treated with advanced glycation end-products (RAGE) or toll-like receptor 4 (TLR4) siRNA prior to rhHMGB1. Proteins lysates were processed for Western blotting for TLR4, RAGE, insulin receptor, Akt, and IRS-1 phosphorylation. We found that rhHMGB1 blocked insulin and Akt phosphorylation through either RAGE or TLR4 actions. Epac1 overcame both endogenous and exogenous HMGB1 to maintain normal insulin signalling. Taken together, these data offer upstream targets to maintain proper insulin signal transduction in the retinal vasculature.
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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.