ArticleScientific reports2018
Blockade of HMGB1 Attenuates Diabetic Nephropathy in Mice.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Ferroptosis and ferritinophagy in diabetes complications.Molecular metabolism · 2022Pooled it
- Mucosal-associated invariant T cells and the gut-kidney axis: a review.Clinical kidney journal · 2026Review
- Advances in the Identification of Novel Urinary Biomarkers for Diabetic Kidney Disease.Journal of diabetes research · 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
- Damage-Associated Molecular Patterns and Pattern Recognition Receptors in the Podocyte.Journal of the American Society of Nephrology : JASN · 2025Review
- Crosstalk between ferroptosis and innate immune in diabetic kidney disease: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Development of a predictive model for the risk of microalbuminuria: comparison of 2 machine learning algorithms.Journal of diabetes and metabolic disorders · 2024Article
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
- Melatonin inhibits circadian gene DEC1 and TLR2/MyD88/NF-κB signaling pathway to alleviate renal injury in type 2 diabetic mice.Acta diabetologica · 2024Article
- [Quercetin ameliorates diabetic kidney injury in rats by inhibiting the HMGB1/RAGE/NF-κB signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Investigating HMGB1 as a potential serum biomarker for early diabetic nephropathy monitoring by quantitative proteomics.iScience · 2024Article
- Interference in the nutrient-sensing and inflammatory signaling pathways by renal autophagy activation in mice with late stage diabetic nephropathy.International urology and nephrology · 2024Article
- High mobility group box 1 (HMGB1) mediates nicotine-induced podocyte injury.Frontiers in pharmacology · 2024Article
- Autophagy inhibitor 3-methyladenine attenuates renal injury in streptozotocin-induced diabetic mice.Iranian journal of basic medical sciences · 2024Article
- Article
- Ferroptosis in diabetic nephropathy: Mechanisms and therapeutic implications.Metabolism open · 2023Review
- Targeting HMGB1: A Potential Therapeutic Strategy for Chronic Kidney Disease.International journal of biological sciences · 2023Review
- Emerging Role of Ferroptosis in Diabetic Kidney Disease: Molecular Mechanisms and Therapeutic Opportunities.International journal of biological sciences · 2023Review
- Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms.Frontiers in endocrinology · 2023Review
- Circular RNAs in Diabetic Nephropathy: Updates and Perspectives.Aging and disease · 2022Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of TLR2 or TLR4 by endogenous ligands such as high mobility group box 1 (HMGB1) may mediate inflammation causing diabetic kidney injury. We determined whether blockade of HMGB1 signaling by: (1) supra-physiological production of endogenous secretory Receptor for Advanced Glycation End-products (esRAGE), a receptor for HMGB1; (2) administration of HMGB1 A Box, a specific competitive antagonist, would inhibit development of streptozotocin induced diabetic nephropathy (DN). Wild-type diabetic mice developed albuminuria, glomerular injuries, interstitial fibrosis and renal inflammation. Using an adeno-associated virus vector, systemic over-expression of esRAGE afforded significant protection from all parameters. No protection was achieved by a control vector which expressed human serum albumin. Administration of A Box was similarly protective against development of DN. To determine the mechanism(s) of protection, we found that whilst deficiency of TLR2, TLR4 or RAGE afforded partial protection from development of DN, over-expression of esRAGE provided additional protection in TLR2
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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.