ArticleJournal of dental research2014
BET Inhibitor JQ1 Blocks Inflammation and Bone Destruction.
Article in Journal of dental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.
- Exploring the Impact of Biological Agents on Protecting Against Experimental Periodontitis: A Systematic Review of Animal-Based Studies.BioMed research international · 2024Pooled it
- A randomized study of the safety and pharmacokinetics of GSK3358699, a mononuclear myeloid-targeted bromodomain and extra-terminal domain inhibitor.British journal of clinical pharmacology · 2022Trial
- Phase 1b study of ABBV-744, a novel, selective BET inhibitor, as monotherapy for patients with myelofibrosis.Blood advances · 2026Article
- BET inhibitors in cardiovascular diseases: from atherosclerosis to heart failure.Pharmacological reports : PR · 2026Review
- Genome-wide profiling of salivary promoter-region DNA methylation in periodontitis: the Tromsø Study.BMC medical genomics · 2026Article
- A comprehensive analysis of epigenetic mechanisms regulating inflammation-induced TNF-α gene expression by small-molecule inhibitor screening.Molecular biology reports · 2026Article
- Molecular time machines unleashed: small-molecule-driven reprogramming to reverse the senescence.Stem cells translational medicine · 2026Review
- Decoding Epigenetic Switches: How Histone Acetylation/Deacetylation Regulates Mononuclear/Macrophage Fate in Bone Disorders.International journal of biological sciences · 2026Review
- Potential Use of VYN202, a Novel Small Molecular Bromodomain and Extra-Terminal Inhibitor, in Mitigating Secondhand Smoke (SHS)-Induced Pulmonary Inflammation.Current issues in molecular biology · 2025Article
- Protein acylation in inflammatory diseases: from mechanisms to therapeutic strategies.Cell communication and signaling : CCS · 2025Review
- Multi-omics based and AI-driven drug repositioning for epigenetic therapy in female malignancies.Journal of translational medicine · 2025Review
- Targeting BRD4 to attenuate RANKL-induced osteoclast activation and bone erosion in rheumatoid arthritis.Molecular and cellular biochemistry · 2025Article
- Bromodomain-containing 4 as a therapeutic target in inflammatory bowel diseases and colorectal cancer.Frontiers in pharmacology · 2025Review
- Protein lysine acetylation regulates oral microorganisms.Frontiers in cellular and infection microbiology · 2025Review
- Bromodomain and Extraterminal Protein Inhibition: A Novel Therapeutic Strategy in Arthritis.Journal of inflammation research · 2025Review
- JQ1 attenuates contrast-induced acute kidney injury through the upregulation of autophagy and inhibition of inflammation.International urology and nephrology · 2024Article
- BET in hematologic tumors: Immunity, pathogenesis, clinical trials and drug combinations.Genes & diseases · 2023Review
- Mapping of DNA methylation-sensitive cellular processes in gingival and periodontal ligament fibroblasts in the context of periodontal tissue homeostasis.Frontiers in immunology · 2023Article
- The Role of Bromodomain and Extraterminal (BET) Proteins in Controlling the Phagocytic Activity of Microglia In Vitro: Relevance to Alzheimer's Disease.International journal of molecular sciences · 2022Article
- The Relevance of DNA Methylation and Histone Modification in Periodontitis: A Scoping Review.Cells · 2022Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
BET proteins are a group of epigenetic regulators controlling transcription through reading acetylated histone tails and recruiting transcription complexes. They are considered as potential therapeutic targets in many distinct diseases. A novel synthetic bromodomain and extraterminal domain (BET) inhibitor, JQ1, was proved to suppress oncogene transcription and inflammatory responses. The present study was aimed to investigate the effects of JQ1 on inflammatory response and bone destruction in experimental periodontitis. We found that JQ1 significantly suppressed lipopolysaccharide (LPS)-stimulated inflammatory cytokine transcription, including interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (TNF-α), as well as receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast markers, such as c-Fos, nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1 (NFATc1), tartrate-resistant acid phosphatase (TRAP) and cathepsin K in vitro. JQ1 also inhibited toll-like receptors 2/4 (TLR2/4) expression and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) phosphorylation and nuclear translocation. Chromatin immunoprecipitation and quantitative polymerase chain reaction (ChIP-qPCR) revealed that JQ1 neutralized BRD4 enrichment at several gene promoter regions, including NF-κB, TNF-α, c-Fos, and NFATc1. In a murine periodontitis model, systemic administration of JQ1 significantly inhibited inflammatory cytokine expression in diseased gingival tissues. Alveolar bone loss was alleviated in JQ1-treated mice because of reduced osteoclasts in periodontal tissues. These unprecedented results suggest the BET inhibitor JQ1 as a prospective new approach for treating periodontitis.
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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.