ReviewJournal of inflammation research2025
Bromodomain and Extraterminal Protein Inhibition: A Novel Therapeutic Strategy in Arthritis.
Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- ATAD2 suppresses senescence and SASP via SIRT7-p53/p21 to drive progression and immune evasion in endometrial cancer.Clinical epigenetics · 2026Article
- Stigmasterol ameliorates Freund's complete adjuvant-induced polyarthritis in rats.Inflammopharmacology · 2026Article
- Bromodomain-containing protein 4 in inflammatory diseases: molecular mechanisms and therapeutic potential.Journal of inflammation (London, England) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arthritis is an inflammatory condition that affects the joints and surrounding tissues, triggered by factors such as inflammation, infection, degeneration, and trauma. The major forms of arthritis include osteoarthritis (OA), rheumatoid arthritis (RA), and gouty arthritis (GA). Its pathogenesis primarily involves synovial inflammation, cartilage degradation, and subchondral bone remodeling, with pro-inflammatory cytokines, collagenases, and other mediators playing central roles in disease onset and progression. The bromodomain and extraterminal (BET) protein family-a subclass of the larger bromodomain protein superfamily-comprises BRD2, BRD3, BRD4, and BRDT. The regulatory functions of BET proteins in inflammation highlight their considerable potential for mitigating arthritis-related pathology. This review provides a comprehensive overview of recent research on the role of BET proteins in OA, RA, and GA, aiming to deepen our understanding of the protective mechanisms of BET inhibitors, underscore their potential as therapeutic targets, and emphasize their relevance in the development of novel treatment strategies.
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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.