ArticleJCI insight2020
BET bromodomain proteins regulate transcriptional reprogramming in genetic dilated cardiomyopathy.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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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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.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Cell Type-Specific Roles for BRD4 in Heart Failure.Current cardiology reports · 2026Review
- BRD4 inhibition mitigates acute and chronic corneal injury following topical nitrogen mustard exposure.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- A Nomogram Integrating Inflammatory Biomarkers and Echocardiographic Parameters for Predicting Left Ventricular Outflow Tract Obstruction Risk in Hypertrophic Cardiomyopathy.Journal of cardiovascular development and disease · 2026Article
- BRD4 contributes to the cytokine-induced acquisition of an IL-13RA2-positive inflammatory fibroblast phenotype.Journal of Crohn's & colitis · 2026Article
- The cardiac 4D nucleome: nuclear and chromatin dynamics across development, disease and ageing.Nature reviews. Cardiology · 2026Review
- Epigenetic Regulation in Dilated Cardiomyopathy.Heart failure clinics · 2026Review
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Cardiac Fibroblasts: Helping or Hurting.Genes · 2025Review
- Article
- Unlocking the secrets of aging: Epigenetic reader BRD4 as the target to combatting aging-related diseases.Journal of advanced research · 2024Review
- BRD4: an effective target for organ fibrosis.Biomarker research · 2024Review
- Epigenetic regulation of cancer-associated fibroblast heterogeneity.Biochimica et biophysica acta. Reviews on cancer · 2023Review
- Emerging epigenetic therapies of cardiac fibrosis and remodelling in heart failure: from basic mechanisms to early clinical development.Cardiovascular research · 2023Review
- Modelling the pathology and treatment of cardiac fibrosis in vascularised atrial and ventricular cardiac microtissues.Frontiers in cardiovascular medicine · 2023Article
- Transcriptional regulation of cardiac fibroblast phenotypic plasticity.Current opinion in physiology · 2022Article
- Therapeutic targets for cardiac fibrosis: from old school to next-gen.The Journal of clinical investigation · 2022Review
- Estrogen signaling as a bridge between the nucleus and mitochondria in cardiovascular diseases.Frontiers in cell and developmental biology · 2022Review
- Article
- BET Protein-Mediated Transcriptional Regulation in Heart Failure.International journal of molecular sciences · 2021Review
- Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
Abstract
The bromodomain and extraterminal (BET) family comprises epigenetic reader proteins that are important regulators of inflammatory and hypertrophic gene expression in the heart. We previously identified the activation of proinflammatory gene networks as a key early driver of dilated cardiomyopathy (DCM) in transgenic mice expressing a mutant form of phospholamban (PLNR9C) - a genetic cause of DCM in humans. We hypothesized that BETs coactivate this inflammatory process, representing a critical node in the progression of DCM. To test this hypothesis, we treated PLNR9C or age-matched WT mice longitudinally with the small molecule BET bromodomain inhibitor JQ1 or vehicle. BET inhibition abrogated adverse cardiac remodeling, reduced cardiac fibrosis, and prolonged survival in PLNR9C mice by inhibiting expression of proinflammatory gene networks at all stages of disease. Specifically, JQ1 had profound effects on proinflammatory gene network expression in cardiac fibroblasts, while having little effect on gene expression in cardiomyocytes. Cardiac fibroblast proliferation was also substantially reduced by JQ1. Mechanistically, we demonstrated that BRD4 serves as a direct and essential regulator of NF-κB-mediated proinflammatory gene expression in cardiac fibroblasts. Suppressing proinflammatory gene expression via BET bromodomain inhibition could be a novel therapeutic strategy for chronic DCM in humans.
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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.