ArticleCommunications biology2024
Brd4 modulates metabolic endotoxemia-induced inflammation by regulating colonic macrophage infiltration in high-fat diet-fed mice.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Microbiota-Mediator-Host Signaling Networks in Metabolic Syndrome: From Mechanistic Insights to Therapeutic Targeting.Microorganisms · 2026Review
- Review
- BRD4 modulates antimicrobial defense via non-canonical NRF2 activation in macrophages to confer protection against sepsis.PLoS pathogens · 2026Article
- Bromodomain-containing protein 4 in inflammatory diseases: molecular mechanisms and therapeutic potential.Journal of inflammation (London, England) · 2026Review
- Integrated single-cell and bulk tissue analyses reveal distinct macrophage subtypes and a candidate prognostic signature in colorectal cancer: implications for tumor immune characterization.Frontiers in immunology · 2026Article
- The gut microbiome-cardiometabolic axis: insights into obesity, type 2 diabetes, and hypertension.Frontiers in endocrinology · 2026Review
- Microbiota-miR-101 interactions in obesity-associated colorectal cancer: from barrier dysfunction to precision therapeutic strategies.Frontiers in pharmacology · 2026Review
- Imidazole propionate ameliorates lipid metabolism in adipocytes to attenuate high-fat diet-induced obesity via PPAR signaling pathway.Lipids in health and disease · 2025Article
- BRD4 regulates PAI-1 expression in tumor-associated macrophages to drive chemoresistance in colorectal cancer.Oncogene · 2025Article
- Unraveling the Role of Metabolic Endotoxemia in Accelerating Breast Tumor Progression.Biomedicines · 2025Article
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10 authors.
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Abstract
High-fat diet (HFD) induces low-grade chronic inflammation, contributing to obesity and insulin resistance. However, the precise mechanisms triggering obesity-associated metabolic inflammation remain elusive. In this study, we identified epigenetic factor Brd4 as a key player in this process by regulating the expression of Ccr2/Ccr5 in colonic macrophage. Upon 4-week HFD, myeloid-lineage-specific Brd4 deletion (Brd4-CKO) mice showed reduced colonic inflammation and macrophage infiltration with decreased expression of Ccr2 and Ccr5. Mechanistically, Brd4 was recruited by NF-κB to the enhancer regions of Ccr2 and Ccr5, promoting enhancer RNA expression, which facilitated Ccr2/Ccr5 expression and macrophage migration. Furthermore, decreased infiltration of Ccr2/Ccr5-positive colonic macrophages in Brd4-CKO mice altered gut microbiota composition and reduced intestinal permeability, thereby lowering metabolic endotoxemia. Finally, Brd4-CKO mice subjected to a 4-week LPS infusion exhibited restored susceptibility to HFD-induced obesity and insulin resistance. This study identifies Brd4 as a critical initiator of colonic macrophage-mediated inflammation and metabolic endotoxemia upon HFD, suggesting Brd4 as a potential target for mitigating HFD-induced inflammation, obesity, and its metabolic complications.
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