ArticleRedox biology2017
HMGB1-RAGE pathway drives peroxynitrite signaling-induced IBD-like inflammation in murine nonalcoholic fatty liver disease.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 66 citations in OpenAlex.
- Toward Specific Detection of Peroxynitrite─Intramolecular Cyclization of Boronobenzylated Pyridinium Probe in Chemical and Cellular Systems.Chemical research in toxicology · 2026Article
- Age- and Sex-dependent Effects of High-fructose, High-fat Diets on Small Bowel Inflammation and Hepatic Steatosis in F344 Rats.Journal of neurogastroenterology and motility · 2025Article
- Inhibition of the HMGB1-RAGE Axis Attenuates Microglial Inflammation and Ameliorates Hypoxia-Induced Cognitive Impairment.International journal of molecular sciences · 2025Article
- The Impact of Recreational Diving to a Depth of 40 m on Selected Intracellular DAMPs.International journal of molecular sciences · 2025Article
- Innovative pH-responsive alginate-coated rosuvastatin-loaded chitosan nanoparticles: a targeted approach to inhibiting HMGB1-activated RAGE/TLR4-NFκB signaling in colonic inflammation in rats.Frontiers in pharmacology · 2025Article
- Immune Microenvironment on the Molecular Mechanisms and Therapeutic Targets of MAFLD.ImmunoTargets and therapy · 2025Review
- Small molecule probes for peroxynitrite detection.Redox biochemistry and chemistry · 2024Article
- HMGB1-Mediated Cell Death-A Crucial Element in Post-Hepatectomy Liver Failure.International journal of molecular sciences · 2024Article
- The RAGE Axis: A Relevant Inflammatory Hub in Human Diseases.Biomolecules · 2024Review
- The emerging role of oxidative stress in inflammatory bowel disease.Frontiers in endocrinology · 2024Review
- Exploration of the core pathway of inflammatory bowel disease complicated with metabolic fatty liver and two-sample Mendelian randomization study of the causal relationships behind the disease.Frontiers in immunology · 2024Article
- Hepatic NLRP3-Derived Hsp70 Binding to TLR4 Mediates MASLD to MASH Progression upon Inhibition of PP2A by Harmful Algal Bloom Toxin Microcystin, a Second Hit.International journal of molecular sciences · 2023Article
- Loss of RAGE prevents chronic intermittent hypoxia-induced nonalcoholic fatty liver disease via blockade of NF-кB pathway.Gene therapy · 2023Article
- Lipid and glucose metabolism in senescence.Frontiers in nutrition · 2023Review
- Molecular insights into the multifaceted functions and therapeutic targeting of high mobility group box 1 in metabolic diseases.Journal of cellular and molecular medicine · 2022Review
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- Serum superoxide dismutase level is a potential biomarker of disease prognosis in patients with HEV-induced liver failure.BMC gastroenterology · 2022Article
- Glycation and a Spark of ALEs (Advanced Lipoxidation End Products) - Igniting RAGE/Diaphanous-1 and Cardiometabolic Disease.Frontiers in cardiovascular medicine · 2022Review
- The immune response as a therapeutic target in non-alcoholic fatty liver disease.Frontiers in immunology · 2022Review
- Using PAMPs and DAMPs as adjuvants in cancer vaccines.Human vaccines & immunotherapeutics · 2021Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Recent clinical studies found a strong association of colonic inflammation and Inflammatory bowel disease (IBD)-like phenotype with NonAlcoholic Fatty liver Disease (NAFLD) yet the mechanisms remain unknown. The present study identifies high mobility group box 1 (HMGB1) as a key mediator of intestinal inflammation in NAFLD and outlines a detailed redox signaling mechanism for such a pathway. NAFLD mice showed liver damage and release of elevated HMGB1 in systemic circulation and increased intestinal tyrosine nitration that was dependent on NADPH oxidase. Intestines from NAFLD mice showed higher Toll like receptor 4 (TLR4) activation and proinflammatory cytokine release, an outcome strongly dependent on the existence of NAFLD pathology and NADPH oxidase. Mechanistically intestinal epithelial cells showed the HMGB1 activation of TLR-4 was both NADPH oxidase and peroxynitrite dependent with the latter being formed by the activation of NADPH oxidase. Proinflammatory cytokine production was significantly blocked by the specific peroxynitrite scavenger phenyl boronic acid (FBA), AKT inhibition and NADPH oxidase inhibitor Apocynin suggesting NADPH oxidase-dependent peroxynitrite is a key mediator in TLR-4 activation and cytokine release via an AKT dependent pathway. Studies to ascertain the mechanism of HMGB1-mediated NADPH oxidase activation showed a distinct role of Receptor for advanced glycation end products (RAGE) as the use of inhibitors targeted against RAGE or use of deformed HMGB1 protein prevented NADPH oxidase activation, peroxynitrite formation, TLR4 activation and finally cytokine release. Thus, in conclusion the present study identifies a novel role of HMGB1 mediated inflammatory pathway that is RAGE and redox signaling dependent and helps promote ectopic intestinal inflammation in NAFLD.
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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.