ArticleGastroenterology2014
Intracellular Hmgb1 inhibits inflammatory nucleosome release and limits acute pancreatitis in mice.
Article in Gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.
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Who cites it
134 citing papers in PubMed, 1 synthesis or guideline pooled it, 205 citations in OpenAlex.
- Fever on hospital admission is associated with increased disease severity and mortality in acute pancreatitis: a systematic review and meta-analysis.Systematic reviews · 2026Pooled it
- Octreotide attenuates pancreatic fibrosis through modulation of the HMGB1-Wnt/β-catenin axis in experimental chronic pancreatitis.Molecular and cellular biochemistry · 2026Article
- Mechanisms of cardiomyocyte dysfunction induced by extracellular histones.Cell death discovery · 2026Article
- Hyperuricemia aggravates acute pancreatitis through CNR1-mediated inflammatory signaling and gut-pancreas axis dysregulation: a multi-omics and clinical study.Scientific reports · 2026Article
- Pharmacological intervention of the HMGB1-pCTS-L axis to ameliorate inflammatory diseases.Frontiers in immunology · 2026Review
- Thrombomodulin Mitigates the Progression of Hepatocellular Carcinoma in Steatotic Liver.Journal of hepatocellular carcinoma · 2026Article
- Post-translational modification crosstalk in acute pancreatitis: linking acinar stress to innate immune amplification and tissue repair.Frontiers in immunology · 2026Review
- EP300 confers protection against acute pancreatitis via acetylating HSF1 and promoting PRKN-mediated mitophagy in pancreatic acinar cells.Cell communication and signaling : CCS · 2025Article
- Mechanism of action of HMGB1 in urologic malignancies.Frontiers in oncology · 2025Review
- Macroautophagy/autophagy promotes resistance to KRASCancer letters · 2024Article
- GV-971 prevents severe acute pancreatitis by remodeling the microbiota-metabolic-immune axis.Nature communications · 2024Article
- High-mobility group box 1 fragment ameliorates chronic pancreatitis induced by caerulein in mice.Journal of gastroenterology · 2024Article
- High-mobility group box 1: friend or foe in pancreatitis.Journal of gastroenterology · 2024Article
- Autophagy and the pancreas: Healthy and disease states.Frontiers in cell and developmental biology · 2024Review
- Identifying the ceRNA Regulatory Network in Early-Stage Acute Pancreatitis and Investigating the Therapeutic Potential of NEAT1 in Mouse Models.Journal of inflammation research · 2024Article
- Eugenol Reduced ΜPO, CD45 and HMGB1 Expression and Attenuated the Expression of Leukocyte Infiltration Markers in the Intestinal Tissue in Biliopancreatic Duct Ligation-Induced Pancreatitis in Rats.Medicina (Kaunas, Lithuania) · 2023Article
- Da-Cheng-Qi decoction improves severe acute pancreatitis-associated acute lung injury by interfering with intestinal lymphatic pathway and reducing HMGB1-induced inflammatory response in rats.Pharmaceutical biology · 2023Article
- The multifunctional protein HMGB1: 50 years of discovery.Nature reviews. Immunology · 2023Review
- Galantamine ameliorates experimental pancreatitis.Molecular medicine (Cambridge, Mass.) · 2023Article
- HMGB1 released by mesothelial cells drives the development of asbestos-induced mesothelioma.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
22 authors at 7 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsHigh mobility group box 1 (HMGB1) is an abundant protein that regulates chromosome architecture and also functions as a damage-associated molecular pattern molecule. Little is known about its intracellular roles in response to tissue injury or during subsequent local and systemic inflammatory responses. We investigated the function of Hmgb1 in mice after induction of acute pancreatitis.
methodsWe utilized a Cre/LoxP system to create mice with pancreas-specific disruption in Hmbg1 (Pdx1-Cre; HMGB1(flox/flox) mice). Acute pancreatitis was induced in these mice (HMGB1(flox/flox) mice served as controls) after injection of l-arginine or cerulein. Pancreatic tissues and acinar cells were collected and analyzed by histologic, immunoblot, and immunohistochemical analyses.
resultsAfter injection of l-arginine or cerulein, Pdx1-Cre; HMGB1(flox/flox) mice developed acute pancreatitis more rapidly than controls, with increased mortality. Pancreatic tissues of these mice also had higher levels of serum amylase, acinar cell death, leukocyte infiltration, and interstitial edema than controls. Pancreatic tissues and acinar cells collected from the Pdx1-Cre; HMGB1(flox/flox) mice after l-arginine or cerulein injection demonstrated nuclear catastrophe with greater nucleosome release when compared with controls, along with increased phosphorylation/activation of RELA nuclear factor κB, degradation of inhibitor of κB, and phosphorylation of mitogen-activated protein kinase. Inhibitors of reactive oxygen species (N-acetyl-l-cysteine) blocked l-arginine-induced DNA damage, necrosis, apoptosis, release of nucleosomes, and activation of nuclear factor κB in pancreatic tissues and acinar cells from Pdx1-Cre; HMGB1(flox/flox) and control mice. Exogenous genomic DNA and recombinant histone H3 proteins significantly induced release of HMGB1 from mouse macrophages; administration of antibodies against H3 to mice reduced serum levels of HMGB1 and increased survival after l-arginine injection.
conclusionsIn 2 mouse models of acute pancreatitis, intracellular HMGB1 appeared to prevent nuclear catastrophe and release of inflammatory nucleosomes to block inflammation. These findings indicate a role for the innate immune response in tissue damage.
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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.