ArticleInternational journal of clinical and experimental pathology2015
HMGB1 is activated in type 2 diabetes mellitus patients and in mesangial cells in response to high glucose.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 37 citations in OpenAlex.
- Serum Advanced Glycation End Products as Drivers of Poor Tendon Outcomes in Diabetes? An Emerging Hypothesis and Narrative Review.Endocrinology, diabetes & metabolism · 2026Review
- The AGE-RAGE-DIAPH1 Axis in Type 2 Diabetes and Metabolic Dysfunction: From Carbonyl Stress to Diabetic Myocardial and Neuronal Injury.International journal of molecular sciences · 2026Review
- Progression of diabetic nephropathy and adverse renal outcomes: possible involvement of Toll-like receptor 4 expression.Clinical and experimental nephrology · 2026Article
- HMGB1: a key molecule linking chronic inflammation to complications in type 2 diabetes mellitus and a target for exercise intervention.Frontiers in endocrinology · 2026Review
- From receptor to response: dissecting the TLR4 pathway in diabetic neuropathy.Inflammopharmacology · 2025Review
- Discovery and serological validation of DAMP-derived B-cell epitopes as diagnostic biomarkers for diabetic nephropathy.Frontiers in endocrinology · 2025Article
- Targeting Macrophages: Therapeutic Approaches in Diabetic Kidney Disease.International journal of molecular sciences · 2024Review
- The role of innate immunity in diabetic nephropathy and their therapeutic consequences.Journal of pharmaceutical analysis · 2024Review
- The inverse association between DNA gaps and HbA1c levels in type 2 diabetes mellitus.Scientific reports · 2023Article
- Targeting HMGB1: A Potential Therapeutic Strategy for Chronic Kidney Disease.International journal of biological sciences · 2023Review
- RAGE signaling regulates the progression of diabetic complications.Frontiers in pharmacology · 2023Review
- The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation.International journal of molecular sciences · 2021Review
- Activation of Peripheral Blood Mononuclear Cells and Leptin Secretion: New Potential Role of Interleukin-2 and High Mobility Group Box (HMGB)1.International journal of molecular sciences · 2021Article
- Expatiating the molecular approaches of HMGB1 in diabetes mellitus: Highlighting signalling pathways via RAGE and TLRs.Molecular biology reports · 2021Review
- Protein Kinases Signaling in Pancreatic Beta-cells Death and Type 2 Diabetes.Advances in experimental medicine and biology · 2021Article
- miR-103a-3p alleviates oxidative stress, apoptosis, and immune disorder in oxygen-glucose deprivation-treated BV2 microglial cells and rats with cerebral ischemia-reperfusion injury by targeting high mobility group box 1.Annals of translational medicine · 2020Article
- Innate immunity in diabetic kidney disease.Nature reviews. Nephrology · 2020Review
- Epigenetic Regulation of S100A9 and S100A12 Expression in Monocyte-Macrophage System in Hyperglycemic Conditions.Frontiers in immunology · 2020Article
- Identification of potential therapeutic target genes in mouse mesangial cells associated with diabetic nephropathy using bioinformatics analysis.Experimental and therapeutic medicine · 2019Article
- Sodium Butyrate Ameliorates Streptozotocin-Induced Type 1 Diabetes in Mice by Inhibiting the HMGB1 Expression.Frontiers in endocrinology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is one of the most devastating complications of diabetes, leading the cause of end-stage renal disease (ESRD). And investigations into mechanisms underlying renal inflammation may provide new insight into novel therapeutic targets for patients with DN. However, little is known about the promotion of inflammation in DN. In the present study, we examined the promotion by high glucose to High-mobility group box-1 (HMGB1) in patients with type 2 diabetes mellitus or in renal mesangial SV40 MES 13 cells. Results demonstrated that high glucose promoted the pre-inflammatory cytokines, such as TNF-α, IL-1β and IL-6 in patients with T2DM or in SV40 MES 13 cells. And the serum HMGB1 was also upregulated in T2DM patients, correlating with serum IL-6 and TNFα. The in vitro results indicated that HMGB1 mediated the D-glucose-induced pro-inflammatory cytokines in mesangial cells. And the NF-κB signaling pathway involved in the promotion of pro-inflammatory cytokines by D-glucose. In summary, the present study indicated that HMGB1 was significantly promoted by the glucose in vivo or in vitro, in an association with an upregulation of pro-inflammatory cytokines, via activating NF-κB signaling pathway. And the strategy of HMGB1 inhibition reduced the upregulation of pro-inflammatory cytokines in response to high glucose, via inhibiting the NF-κB signaling pathway. It implies the regulatory role of HMGB1 in the inflammatory responses in DN.
Indexed as
Identifiers
26261550PMC4525884W1139006711What OpenQuestion holds
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.