ArticleNature communications2018
Endothelial deletion of Ino80 disrupts coronary angiogenesis and causes congenital heart disease.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 95 citations in OpenAlex.
- Endocardial transcription factor HAND2 orchestrates hypoxic and TGF-β signaling to modulate coronary artery formation.The Journal of clinical investigation · 2026Article
- Cardiac Organoids for Modeling Congenital Heart Disease: From Genetic Discovery to Therapeutic Screening.Current cardiology reports · 2026Review
- Rethinking Left Ventricular Noncompaction and Excessive Left Ventricular Trabeculation: Development, Genetics, and a Proposed Conceptual Framework.Journal of clinical medicine · 2026Review
- Cardiomyocyte-Specific bcl11b Knockout Causes Left Ventricular Noncompaction by Dysregulating pou3f2 and Titin.International journal of molecular sciences · 2026Article
- SOX6 is expressed in various cell lineages in the developing mouse heart and contributes to proper valvuloseptal development.Anatomical record (Hoboken, N.J. : 2007) · 2026Article
- The Prion-Like Properties of the INO80 Chromatin Remodeler Regulate Metabolic Gene Expression.bioRxiv : the preprint server for biology · 2026Article
- TM4SF1 mediates YAP/TAZ regulation of coronary artery formation.Scientific reports · 2026Article
- Left Ventricular Hypertrabeculation and Ventricular Arrhythmias.Journal of clinical medicine · 2026Article
- Modeling embryonic heart vascular plexus development and sympathetic innervation on a human heart organoid.iScience · 2026Article
- Ets1-regulated endothelial-secreted factors promote compact myocardial growth and contribute to the pathogenesis of ventricular non-compaction.Cardiovascular research · 2026Article
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- Developmental single-cell atlas of coronary vessel growth and cardiomyocyte interaction in zebrafish.Development (Cambridge, England) · 2026Article
- INO80 regulates promoter-associated R-loops to coordinate transcription and maintain genome stability in embryonic stem cells.Biological research · 2026Article
- Defects inFrontiers in genetics · 2026Article
- Hypercortisolism with coronary nonobstructive myocardial infarction and left ventricular noncompaction: a case report.Frontiers in cardiovascular medicine · 2026Article
- Preliminary investigation into the mechanical implications of excessive trabecularization in the left ventricle.Quantitative imaging in medicine and surgery · 2025Article
- Article
- Emerging Epigenetic Therapies for the Treatment of Cardiac Fibrosis.Biomedicines · 2025Review
- The trabecular and compact myocardium of adult vertebrate ventricles are transcriptionally similar despite morphological differences.Annals of the New York Academy of Sciences · 2025Article
- Establishment and functional studies of a model of cardiomyopathy with cardiomyocyte-specific conditional knockout of Arhgef18.Disease models & mechanisms · 2025Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
During development, the formation of a mature, well-functioning heart requires transformation of the ventricular wall from a loose trabecular network into a dense compact myocardium at mid-gestation. Failure to compact is associated in humans with congenital diseases such as left ventricular non-compaction (LVNC). The mechanisms regulating myocardial compaction are however still poorly understood. Here, we show that deletion of the Ino80 chromatin remodeler in vascular endothelial cells prevents ventricular compaction in the developing mouse heart. This correlates with defective coronary vascularization, and specific deletion of Ino80 in the two major coronary progenitor tissues-sinus venosus and endocardium-causes intermediate phenotypes. In vitro, endothelial cells promote myocardial expansion independently of blood flow in an Ino80-dependent manner. Ino80 deletion increases the expression of E2F-activated genes and endothelial cell S-phase occupancy. Thus, Ino80 is essential for coronary angiogenesis and allows coronary vessels to support proper compaction of the heart wall.
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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.