ArticleActa pharmacologica Sinica2024
Cardiac-specific deletion of BRG1 ameliorates ventricular arrhythmia in mice with myocardial infarction.
Article in Acta pharmacologica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 6 citations in OpenAlex.
- Epigenetic and chromatin remodeling mechanisms across cardiomyopathies: a comprehensive review.Epigenetics & chromatin · 2026Review
- Identification of key biomarkers for myocardial infarction by multi-omics analysis and machine learning.Frontiers in immunology · 2026Article
- ID2 attenuates post-MI ventricular arrhythmias by targeting GATA4 suppression to preserve mitochondrial function and NaOpen medicine (Warsaw, Poland) · 2026Article
- Establishment and validation of a risk prediction model for malignant ventricular arrhythmia in acute myocardial infarction patients based on 24-hour dynamic electrocardiogram parameters.American journal of translational research · 2026Article
- BRG1 exacerbates myocardial fibrosis after myocardial infarction by interacting with ZEB1.Frontiers in pharmacology · 2026Article
- NMDA-Type Glutamate Receptor Activation Promotes Ischemic Arrhythmias by Targeting the AKT1-TBX3-Nav1.5 Axis.Acta physiologica (Oxford, England) · 2025Article
- Brg1 and RUNX1 synergy in regulating TRPM4 channel in mouse cardiomyocytes.Frontiers in pharmacology · 2024Article
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19 authors at 1 institution in 1 country.
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Abstract
Malignant ventricular arrhythmia (VA) after myocardial infarction (MI) is mainly caused by myocardial electrophysiological remodeling. Brahma-related gene 1 (BRG1) is an ATPase catalytic subunit that belongs to a family of chromatin remodeling complexes called Switch/Sucrose Non-Fermentable Chromatin (SWI/SNF). BRG1 has been reported as a molecular chaperone, interacting with various transcription factors or proteins to regulate transcription in cardiac diseases. In this study, we investigated the potential role of BRG1 in ion channel remodeling and VA after ischemic infarction. Myocardial infarction (MI) mice were established by ligating the left anterior descending (LAD) coronary artery, and electrocardiogram (ECG) was monitored. Epicardial conduction of MI mouse heart was characterized in Langendorff-perfused hearts using epicardial optical voltage mapping. Patch-clamping analysis was conducted in single ventricular cardiomyocytes isolated from the mice. We showed that BRG1 expression in the border zone was progressively increased in the first week following MI. Cardiac-specific deletion of BRG1 by tail vein injection of AAV9-BRG1-shRNA significantly ameliorated susceptibility to electrical-induced VA and shortened QTc intervals in MI mice. BRG1 knockdown significantly enhanced conduction velocity (CV) and reversed the prolonged action potential duration in MI mouse heart. Moreover, BRG1 knockdown improved the decreased densities of Na
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