ArticleInternational journal of molecular medicine2020
HMGB1 participates in LPS‑induced acute lung injury by activating the AIM2 inflammasome in macrophages and inducing polarization of M1 macrophages via TLR2, TLR4, and RAGE/NF‑κB signaling pathways.
Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 101 papers, 1 of them a synthesis that pooled it.
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Who cites it
101 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Elevated HMGB1 Levels in Neonates With Bronchopulmonary Dysplasia: A Systematic Review and Meta-Analysis.Canadian respiratory journal · 2026Pooled it
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- Discovery of Novel Small-Molecule Toll-like Receptor 2 Agonists via a Scaffold Hopping Strategy.ACS medicinal chemistry letters · 2026Article
- Electroacupuncture pretreatment alleviates myocardial ischemia/reperfusion-induced lung injury by inhibiting the expression of HMGB1/RAGE in male rats.Physiological reports · 2026Article
- Picroside II as a Potential Anti-Inflammatory Agent.Pharmaceutics · 2026Review
- NMI Promotes Pro-Inflammatory Macrophage Polarization and Exacerbates.Inflammation · 2026Article
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Dahuang-mudanpi decoction mitigates ALI/ARDS pulmonary inflammation via multi-target regulation of HMGB1.Frontiers in pharmacology · 2026Article
- Screening and Targeting the HMGB1/RAGE Axis via Proteomics to Alleviate Inflammatory Responses in aJournal of inflammation research · 2026Article
- Role of dual specificity phosphatase 1 in influencing inflammatory pathways in macrophages modulated byFrontiers in immunology · 2026Article
- Targeting Macrophage-Mediated Mechanisms in Sepsis-Induced Cardiomyopathy: From Pathophysiology to Therapeutic Strategies.Journal of inflammation research · 2026Review
- B. adolescentis alleviates inflammation and suppresses PGE2 through remodling gut microbiota to attenuate pulmonary fibrosis in aging mice.NPJ science of food · 2025Article
- Cracking the code of cancer immunotherapy resistance: emerging roles of pyroptosis and necroptosis.Journal of experimental & clinical cancer research : CR · 2025Review
- Endothelial HMGB1-AIM2 axis worsens myocardial ischemia-reperfusion injury by regulating endothelial pyroptosis.Apoptosis : an international journal on programmed cell death · 2025Article
- CpG-A induces liquid-liquid phase separation of HMGB1 to activate the RAGE-mediated inflammatory pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Methylene Blue Alleviates Inflammatory and Oxidative Lung Injury in a Rat Model of Feces-Induced Peritonitis.Medicina (Kaunas, Lithuania) · 2025Article
- Human iPSC-based breast cancer model identifies S100P-dependent cancer stemness induced byScience advances · 2025Article
- Role of Dual Specificity Phosphatase 1 (DUSP1) in influencing inflammatory pathways in macrophages modulated bybioRxiv : the preprint server for biology · 2025Article
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- Verteporfin-Mediated In Situ Nanovaccine Based on Local Conventional-Dose Hypofractionated Radiotherapy Enhances Antitumor and Immunomodulatory Effect.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High mobility group box 1 (HMGB1), a crucial proinflammatory cytokine, was reported to activate the absent in melanoma 2 (AIM2) inflammasome, which are both essential in acute lung injury (ALI). However, their interaction mechanism has remained elusive. Macrophages are known to express the AIM2 inflammasome and the main receptors [receptor for advanced glycation end products (RAGE), Toll‑like receptor 2/4 (TLR‑2/TLR‑4)] of HMGB1 to transmit intracellular signals. The present study aimed to indicate whether HMGB1 participates in the process of lipopolysaccharides (LPS)‑induced ALI through activating the AIM2 inflammasome in macrophages, as well as inducing polarization of M1 macrophages via TLR2, TLR4 and RAGE/ nuclear factor‑κB (NF‑κB) signaling pathways. In an in vivo mouse model of LPS‑induced ALI, anti‑HMGB1, recombinant (r)HMGB1, LPS from Rhodobacter sphaeroides (LPS‑RS, TLR2/4 antagonist) or FPS‑ZM1 (RAGE antagonist) were administrated. In in vitro studies, bone marrow‑derived macrophages from mice primed with LPS were stimulated with or without anti‑HMGB1, rHMGB1, LPS‑RS, or FPS‑ZM1. The findings revealed that anti‑HMGB1, LPS‑RS and FPS‑ZM1 significantly decreased infiltration of inflammatory cells, wet‑to‑dry ratio, myeloperoxidase activity in the lung, the levels of cytokines, as well as macrophages and neutrophil infiltration in the bronchoalveolar lavage fluid. However, rHMGB1 aggravated the inflammatory response in ALI. Mechanistically, anti‑HMGB1, LPS‑RS and FPS‑ZM1 attenuated activation of TLR2, TLR4, and RAGE/NF‑κB signaling pathways and expression of the AIM2 inflammasome in macrophages. However, rHMGB1 enhanced their expression levels and induced polarization of M1 macrophages. These results indicated that HMGB1 could participate in the pathogenesis of ALI by activating the AIM2 inflammasome in macrophages, as well as inducing polarization of M1 macrophages through TLR2, TLR4 and RAGE/NF‑κB signaling pathways.
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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.