ArticleMolecular biology of the cell2017
HMGB1 translocation and release mediate cigarette smoke-induced pulmonary inflammation in mice through a TLR4/MyD88-dependent signaling pathway.
Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 68 citations in OpenAlex.
- Ginger-derived nanoparticles targeting NF-κB mediated inflammatory pathways: a systematic review of in vitro and in vivo evidence.Future science OA · 2026Review
- The NF-κB Signalling Pathway: Mechanisms, Consequences and Therapeutic Targets.Journal of cellular and molecular medicine · 2026Review
- SIRT1 regulates cigarette smoke extract‑induced alveolar macrophage polarization and inflammation by inhibiting the TRAF6/NLRP3 signaling pathway.Molecular medicine reports · 2025Article
- Snhg14/miR-181a-5p axis-mediated "M1" macrophages aggravate LPS-induced myocardial cell injury.Heliyon · 2024Article
- Oral administration of crocin-loaded solid lipid nanoparticles inhibits neuroinflammation in a rat model of epileptic seizures by activating SIRT1 expression.Research in pharmaceutical sciences · 2024Article
- Review
- Therapeutic Potentials of MicroRNA-126 in Cerebral Ischemia.Molecular neurobiology · 2023Review
- TSLP and HMGB1: Inflammatory Targets and Potential Biomarkers for Precision Medicine in Asthma and COPD.Biomedicines · 2023Review
- Regulation of the MyD88 gene in chicken spleen inflammation induced by stress.Journal of animal science · 2023Article
- Hepatocyte-specific regulation of autophagy and inflammasome activation via MyD88 during lethalFrontiers in immunology · 2023Article
- Inflammation-related signaling pathways in tendinopathy.Open life sciences · 2023Review
- The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke-induced inflammation in chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2022Review
- [Long noncoding RNA ZEB1-AS1 aggravates cerebral ischemia/reperfusion injury in rats through the HMGB1/TLR-4 signaling axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Stretch Causes Cell Stress and the Downregulation of Nrf2 in Primary Amnion Cells.Biomolecules · 2022Article
- High Mobility Group Box 1: Biological Functions and Relevance in Oxidative Stress Related Chronic Diseases.Cells · 2022Review
- Epithelial microRNA-30a-3p targets RUNX2/HMGB1 axis to suppress airway eosinophilic inflammation in asthma.Respiratory research · 2022Article
- Muscone improves hypoxia/reoxygenation (H/R)-induced neuronal injury by blocking HMGB1/TLR4/NF-κB pathwayPeerJ · 2022Article
- Cigarette Smoke Condensate Exposure Induces Receptor for Advanced Glycation End-Products (RAGE)-Dependent Sterile Inflammation in Amniotic Epithelial Cells.International journal of molecular sciences · 2021Article
- Magnesium sulfate ameliorates sepsis-induced diaphragm dysfunction in rats via inhibiting HMGB1/TLR4/NF-κB pathway.Neuroreport · 2020Article
- Cigarette smoke-induced HMGB1 translocation and release contribute to migration and NF-κB activation through inducing autophagy in lung macrophages.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We performed studies to determine the role of high-mobility group box 1 (HMGB1) in cigarette smoke (CS)-induced pulmonary inflammation. After mice were exposed to five cigarettes four times a day for 3 d, toll-like receptor 4 (TLR4) expression and TLR4-mediated signaling were significantly up-regulated, and HMGB1 had translocated from the nucleus to the cytoplasm in lung epithelial cells and then been released into the extracellular lung space. On CS exposure, inflammatory cell recruitment and proinflammatory cytokine production were significantly increased in lung tissue and bronchoalveolar lavage, and these effects depended on the TLR4 signaling pathway. HMGB1 inhibition decreased the CS-induced inflammatory response, whereas treatment with exogenous HMGB1 aggravated the damage and increased the phosphorylation of JNK, p38, and IκBα in the lungs of wild-type mice but not in TLR4-knockout mice. Blockade of TLR4 action or TLR4 knockout significantly inhibited HMGB1-induced proinflammatory cytokine production in mouse tracheal epithelial (MTE) cells and lung tissues. In addition, a MyD88 deficiency inhibited JNK, p38, and IκBα phosphorylation, and this effect was associated with the suppressed production of TNF-α and IL-1β in MTE cells and lung tissues in response to CS stimulation. Thus HMGB1 activates the NF-κB and JNK/p38 pathways through TLR4/MyD88-dependent signaling and induces an inflammatory response in lungs exposed to CS.
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