ArticleNature communications2025
Mechanically activated snai1b coordinates the initiation of myocardial delamination for trabeculation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Vein graft failure: Pathophysiology, detection, prevention and emerging therapeutic strategies.Pharmacological reviews · 2026Review
- A Continuum of Atrial Peristalsis Initiates the Bicuspid to Quadricuspid Valve Transition.bioRxiv : the preprint server for biology · 2026Article
- Photoaged microplastics disrupt endothelial stretch-sensitive ion channels to impair calcium signaling and vascular integrity.bioRxiv : the preprint server for biology · 2026Article
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14 authors.
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Abstract
During development, myocardial contractile force and intracardiac hemodynamic shear stress coordinate the initiation of trabeculation. While Snail family genes are well-recognized transcription factors of epithelial-to-mesenchymal transition, snai1b-positive cardiomyocytes are sparsely distributed in the ventricle of zebrafish at 4 days post-fertilization. Isoproterenol treatment significantly increases the number of snai1b-positive cardiomyocytes, of which 80% are Notch-negative. CRISPR-activation of snai1b leads to 51.6% cardiomyocytes forming trabeculae, whereas CRISPR-repression reduces trabecular cardiomyocytes to 6.7% under isoproterenol. In addition, 36.7% of snai1b-repressed cardiomyocytes undergo apical delamination. 4-D strain analysis demonstrates that isoproterenol increases the myocardial strain along radial trabecular ridges in alignment with the snai1b expression and Notch-ErbB2-mediated trabeculation. Single-cell and spatial transcriptomics reveal that these snai1b-positive cardiomyocytes are devoid of some epithelial-to-mesenchymal transition-related phenotypes, such as Col1a2 production and induction by ErbB2 or TGF-β. Thus, we uncover snai1b-positive cardiomyocytes that are mechanically activated to initiate delamination for cardiac trabeculation.
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