ArticleFEBS open bio2018
Degradation of histone deacetylase 4 via the TLR4/JAK/STAT1 signaling pathway promotes the acetylation of high mobility group box 1 (HMGB1) in lipopolysaccharide-activated macrophages.
Article in FEBS open bio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Comparison of Cardioprotective Effects of Propofol versus Sevoflurane in Pediatric Living Donor Liver Transplantation.Annals of transplantation · 2020Trial
- A Novel Role of the LINC01270/miR-326/LDOC1 Axis in Proinflammatory Response Regulation via STAT1 Modulation in THP-1 Cells.International journal of molecular sciences · 2026Article
- Oxidative stress in acute pancreatitis induced acute lung injury: mechanisms and therapeutic advances.PeerJ · 2026Review
- Molecular mechanisms and functions of protein acetylation in sepsis and sepsis-associated organ dysfunction.Cellular & molecular biology letters · 2025Review
- HMGB1 as an extracellular pro-inflammatory cytokine: Implications for drug-induced organic damage.Cell biology and toxicology · 2024Review
- Roles of Histone Deacetylase 4 in the Inflammatory and Metabolic Processes.Diabetes & metabolism journal · 2024Review
- High-mobility group box 1 emerges as a therapeutic target for asthma.Immunity, inflammation and disease · 2023Review
- HAT- and HDAC-Targeted Protein Acetylation in the Occurrence and Treatment of Epilepsy.Biomedicines · 2022Review
- MicroRNA-23a-3p targeting of HMGB1 inhibits LPS-induced inflammation in murine macrophagesExperimental and therapeutic medicine · 2022Article
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- Epigenomic and transcriptomic analyses reveal differences between low-grade inflammation and severe exhaustion in LPS-challenged murine monocytes.Communications biology · 2022Article
- microRNA-124-3p attenuates myocardial injury in sepsis via modulating SP1/HDAC4/HIF-1α axis.Cell death discovery · 2022Article
- Revealing potential diagnostic gene biomarkers of septic shock based on machine learning analysis.BMC infectious diseases · 2022Article
- SP1 Promotes HDAC4 Expression and Inhibits HMGB1 Expression to Reduce Intestinal Barrier Dysfunction, Oxidative Stress, and Inflammatory Response after Sepsis.Journal of innate immunity · 2022Article
- Review: The role of HMGB1 in spinal cord injury.Frontiers in immunology · 2022Review
- Melatonin Ameliorates Lipopolysaccharide-Induced Microglial Inflammation via Triggering SIRT1/HMGB1 Signaling Axis.Journal of molecular neuroscience : MN · 2021Article
- Inhaled [D-AlaJournal of immunology research · 2021Article
- Role of HMGB1 in Chemotherapy-Induced Peripheral Neuropathy.International journal of molecular sciences · 2020Review
- LPS Induces Active HMGB1 Release From Hepatocytes Into Exosomes Through the Coordinated Activities of TLR4 and Caspase-11/GSDMD Signaling.Frontiers in immunology · 2020Article
- Ethyl pyruvate attenuates ventilation-induced diaphragm dysfunction through high-mobility group box-1 in a murine endotoxaemia model.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High mobility group box 1 (HMGB1) has been proposed as crucial in the pathogenesis of many diseases including sepsis. Acetylation of HMGB1 prevents its entry into the nucleus and leads to its secretion from the cell where it can trigger inflammation. We hypothesized that histone deacetylase 4 (HDAC4) controls the acetylation of HMGB1 in lipopolysaccharide (LPS)-stimulated RAW264.7 cells via the janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway. The results showed that LPS treatment promoted the degradation of HDAC4 in a proteasome-dependent manner, which led to HMGB1 acetylation. In LPS-activated RAW264.7 cells, treatment with TAK-242 (a toll like receptor 4 inhibitor) and pyridone 6 (a JAK inhibitor) significantly inhibited HDAC4 degradation and acetylation of HMGB1, and thus prevented secretion of HMGB1. Decreased phosphorylation of STAT1 was also observed. Interestingly, HDAC4 overexpression significantly prevented the acetylation and secretion of HMGB1 in both RAW264.7 cells and isolated murine peritoneal macrophages. We conclude that HDAC4 might be a useful target for the treatment of sepsis.
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