ArticleDevelopmental cell2023
Prerequisite endocardial-mesenchymal transition for murine cardiac trabecular angiogenesis.
Article in Developmental cell, 2023. 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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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Endocardial transcription factor HAND2 orchestrates hypoxic and TGF-β signaling to modulate coronary artery formation.The Journal of clinical investigation · 2026Article
- Transcriptional dynamics of the murine heart during perinatal development at single-cell resolution.Biology open · 2026Article
- Aberrant Phase Separation of Endothelial MAML1 Causes Congenital Heart Disease by Suppressing Notch Activity.Circulation · 2026Article
- Mechanically activated snai1b coordinates the initiation of myocardial delamination for trabeculation.Nature communications · 2025Article
- A Machine Learning-Based Diagnostic Nomogram for Moyamoya Disease: The Validation of Hypoxia-Immune Gene Signatures.Bioengineering (Basel, Switzerland) · 2025Article
- GPAT4 sustains endoplasmic reticulum homeostasis in endocardial cells and safeguards heart development.Nature communications · 2025Article
- Coronary microcirculation dysfunction causing ischemia with non-obstructive coronary arteries: a case report.Frontiers in cardiovascular medicine · 2025Article
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
Coronary heart disease damages the trabecular myocardium, and the regeneration of trabecular vessels may alleviate ischemic injury. However, the origins and developmental mechanisms of trabecular vessels remain unknown. Here, we show that murine ventricular endocardial cells generate trabecular vessels through an "angioEMT" mechanism. Time course fate mapping defined a specific wave of trabecular vascularization by ventricular endocardial cells. Single-cell transcriptomics and immunofluorescence identified a subpopulation of ventricular endocardial cells that underwent endocardial-mesenchymal transition (EMT) before these cells generated trabecular vessels. Ex vivo pharmacological activation and in vivo genetic inactivation experiments identified an EMT signal in ventricular endocardial cells involving SNAI2-TGFB2/TGFBR3, which was a prerequisite for later trabecular-vessel formation. Additional loss- and gain-of-function genetic studies showed that VEGFA-NOTCH1 signaling regulated post-EMT trabecular angiogenesis by ventricular endocardial cells. Our finding that trabecular vessels originate from ventricular endocardial cells through a two-step angioEMT mechanism could inform better regeneration medicine for coronary heart disease.
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