ArticleCirculation2017
High-Resolution Mapping of Chromatin Conformation in Cardiac Myocytes Reveals Structural Remodeling of the Epigenome in Heart Failure.
Article in Circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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Who cites it
110 citing papers in PubMed, 155 citations in OpenAlex.
- Next-generation molecular imaging of cardiac fibrosis.The international journal of cardiovascular imaging · 2026Review
- The cardiac 4D nucleome: nuclear and chromatin dynamics across development, disease and ageing.Nature reviews. Cardiology · 2026Review
- Review
- CTCF Regulates Erythroid Differentiation Through Control of Core Erythroid Transcription Factors.Biomolecules · 2026Article
- Epigenetics, Modifiers, and Molecular Noise: Rethinking Pathophysiology in Dilated and Hypertrophic Cardiomyopathies.International journal of molecular sciences · 2026Review
- Chamber-specific chromatin architecture guides functional interpretation of disease-associated Cis-regulatory elements in human cardiomyocytes.Nature communications · 2026Article
- Chromatin structural gene expression stratifies cardiac cell populations in health and disease.Epigenetics · 2025Article
- CTCF Mediates the Cis-Regulatory Hubs in Mouse Hearts.International journal of molecular sciences · 2025Article
- Review
- Novel insights into post-myocardial infarction cardiac remodeling through algorithmic detection of cell-type composition shifts.PLoS genetics · 2025Article
- A 3D Genome Atlas of Genetic Variants and Their Pathological Effects in Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CTCF Point Mutation at R567 Disrupts Mouse Heart Development via 3D Genome Rearrangement and Transcription Dysregulation.Cell proliferation · 2025Article
- Genetic factors mediating long-range enhancer-promoter communication in mammalian development.Current opinion in genetics & development · 2025Review
- Discovery of therapeutic targets in cardiovascular diseases using high-throughput chromosome conformation capture (Hi-C).Frontiers in genetics · 2025Review
- Chronic intermittent hypoxia exacerbates isoproterenol-induced cardiac hypertrophy and apoptosis.Frontiers in cardiovascular medicine · 2025Article
- Advances in mechanotransduction and sonobiology: effects of audible acoustic waves and low-vibration stimulations on mammalian cells.Biophysical reviews · 2024Review
- Rapid onset fibrotic remodeling and ventricular dysfunction induced by phenylephrine involve targeted reprogramming of myocyte and fibroblast transcriptomes.bioRxiv : the preprint server for biology · 2024Article
- CTCF mutation at R567 causes developmental disorders via 3D genome rearrangement and abnormal neurodevelopment.Nature communications · 2024Article
- Review
- TAD boundary deletion causes PITX2-related cardiac electrical and structural defects.Nature communications · 2024Article
50 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundCardiovascular disease is associated with epigenomic changes in the heart; however, the endogenous structure of cardiac myocyte chromatin has never been determined.
methodsTo investigate the mechanisms of epigenomic function in the heart, genome-wide chromatin conformation capture (Hi-C) and DNA sequencing were performed in adult cardiac myocytes following development of pressure overload-induced hypertrophy. Mice with cardiac-specific deletion of CTCF (a ubiquitous chromatin structural protein) were generated to explore the role of this protein in chromatin structure and cardiac phenotype. Transcriptome analyses by RNA-seq were conducted as a functional readout of the epigenomic structural changes.
resultsDepletion of CTCF was sufficient to induce heart failure in mice, and human patients with heart failure receiving mechanical unloading via left ventricular assist devices show increased CTCF abundance. Chromatin structural analyses revealed interactions within the cardiac myocyte genome at 5-kb resolution, enabling examination of intra- and interchromosomal events, and providing a resource for future cardiac epigenomic investigations. Pressure overload or CTCF depletion selectively altered boundary strength between topologically associating domains and A/B compartmentalization, measurements of genome accessibility. Heart failure involved decreased stability of chromatin interactions around disease-causing genes. In addition, pressure overload or CTCF depletion remodeled long-range interactions of cardiac enhancers, resulting in a significant decrease in local chromatin interactions around these functional elements.
conclusionsThese findings provide a high-resolution chromatin architecture resource for cardiac epigenomic investigations and demonstrate that global structural remodeling of chromatin underpins heart failure. The newly identified principles of endogenous chromatin structure have key implications for epigenetic therapy.
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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.