ArticleEuropean heart journal2021
Endocardial/endothelial angiocrines regulate cardiomyocyte development and maturation and induce features of ventricular non-compaction.
Article in European heart journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 65 citations in OpenAlex.
- Endocardial transcription factor HAND2 orchestrates hypoxic and TGF-β signaling to modulate coronary artery formation.The Journal of clinical investigation · 2026Article
- Rethinking Left Ventricular Noncompaction and Excessive Left Ventricular Trabeculation: Development, Genetics, and a Proposed Conceptual Framework.Journal of clinical medicine · 2026Review
- Coronary endothelial cells receive Notch1 signal during heart development.Biochemistry and biophysics reports · 2026Article
- The Prion-Like Properties of the INO80 Chromatin Remodeler Regulate Metabolic Gene Expression.bioRxiv : the preprint server for biology · 2026Article
- Integrative circulatory engineering for regenerative therapy: Dynamic perfusion design and metabolic maturation in cardiac tissue engineering.Regenerative therapy · 2026Article
- The RNA-binding protein SRSF3 controls epicardial formation by regulating splicing and proliferation.Development (Cambridge, England) · 2026Article
- Ets1-regulated endothelial-secreted factors promote compact myocardial growth and contribute to the pathogenesis of ventricular non-compaction.Cardiovascular research · 2026Article
- Adgrg6/Gpr126 is required for compact wall integrity and establishing trabecular identity during cardiac trabeculation.Nature communications · 2026Article
- Cell-free strategies for cardiomyocyte proliferation and heart repair.Pharmacological reports : PR · 2026Review
- Developmental single-cell atlas of coronary vessel growth and cardiomyocyte interaction in zebrafish.Development (Cambridge, England) · 2026Article
- When ISG15 is involved in inflammation.Frontiers in immunology · 2026Review
- mExperimental & molecular medicine · 2025Review
- Beneficial effects of vascular endothelial growth factor B gene transfer in the aged heart.Cardiovascular research · 2025Article
- 3D-Printed Myocardium-Specific Structure Enhances Maturation and Therapeutic Efficacy of Engineered Heart Tissue in Myocardial Infarction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Throwing thrombi: noncompaction cardiomyopathy causing renal infarct and catastrophic stroke - a case report.BMC cardiovascular disorders · 2025Article
- Histone H2A.Z Deacetylation and Dedifferentiation in Infarcted/Tip60-depleted Cardiomyocytes.bioRxiv : the preprint server for biology · 2025Article
- Insulin-like growth factor family and its impact on pulmonary arterial hypertension: a review.Frontiers in physiology · 2025Review
- Identification of key genes in periodontitis.Frontiers in genetics · 2025Article
- Left Ventricular Non-Compaction: Evolving Concepts.Journal of clinical medicine · 2024Review
- Generation and characterisation of scalable and stable human pluripotent stem cell-derived microvascular-like endothelial cells for cardiac applications.Angiogenesis · 2024Article
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20 authors at 2 institutions in 1 country.
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Abstract
aimsNon-compaction cardiomyopathy is a devastating genetic disease caused by insufficient consolidation of ventricular wall muscle that can result in inadequate cardiac performance. Despite being the third most common cardiomyopathy, the mechanisms underlying the disease, including the cell types involved, are poorly understood. We have previously shown that endothelial cell-specific deletion of the chromatin remodeller gene Ino80 results in defective coronary vessel development that leads to ventricular non-compaction in embryonic mouse hearts. We aimed to identify candidate angiocrines expressed by endocardial and endothelial cells (ECs) in wildtype and LVNC conditions in Tie2Cre;Ino80fl/fltransgenic embryonic mouse hearts, and test the effect of these candidates on cardiomyocyte proliferation and maturation. METHODS AND
resultsWe used single-cell RNA-sequencing to characterize endothelial and endocardial defects in Ino80-deficient hearts. We observed a pathological endocardial cell population in the non-compacted hearts and identified multiple dysregulated angiocrine factors that dramatically affected cardiomyocyte behaviour. We identified Col15a1 as a coronary vessel-secreted angiocrine factor, downregulated by Ino80-deficiency, that functioned to promote cardiomyocyte proliferation. Furthermore, mutant endocardial and endothelial cells up-regulated expression of secreted factors, such as Tgfbi, Igfbp3, Isg15, and Adm, which decreased cardiomyocyte proliferation and increased maturation.
conclusionsThese findings support a model where coronary endothelial cells normally promote myocardial compaction through secreted factors, but that endocardial and endothelial cells can secrete factors that contribute to non-compaction under pathological conditions.
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