ArticleEMBO molecular medicine2026
Histone demethylase KDM4B epigenetically controls NLRP3 expression to enhance inflammatory responses.
Article in EMBO molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Sennoside A Ameliorates Myocardial Fibrosis After Myocardial Infarction by Binding to KDM4B and Regulates IRX2 Expression.Cardiovascular drugs and therapy · 2026Article
- Updates on the role of epigenetics in familial mediterranean fever (FMF).Orphanet journal of rare diseases · 2024Review
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Authors and funding
15 authors.
Funding
Abstract
NLRP3 inflammasome, the archetypical molecular driver of inflammation, plays crucial roles in host defense and maintaining cellular homeostasis. Demethylation of histone 3 lysine 9 trimethylation (H3K9me3, the repressive mark for euchromatic genes) is essential for activating gene transcription. However, whether H3K9 demethylation is required for the induction of proinflammatory cytokines remains largely unknown. Here, we show that histone demethylase lysine-specific demethylase 4B (KDM4B) mediates H3K9me3 demethylation at the Nlrp3 promoter to induce NLRP3 expression, thereby selectively enhancing NLRP3 inflammasome activation without affecting NF-κB activation. Concordantly, both Kdm4b deficiency and the selective KDM4 inhibitor ML324 inhibit NLRP3 inflammasome activation and ameliorate NLRP3-dependent inflammatory diseases in vivo. Furthermore, high glucose level upregulates KDM4B, promoting NLRP3 inflammasome activation and IL-1β secretion, thus aggravating aberrant inflammation during viral infections. Our findings reveal the role of H3K9me3 demethylation in initiating inflammation, identify KDM4B as an epigenetic accelerator of NLRP3, and propose that modulating H3K9me3 could represent a targeted anti-inflammatory strategy.
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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.