ArticleNature communications2024
NOTCH1 mitochondria localization during heart development promotes mitochondrial metabolism and the endothelial-to-mesenchymal transition in mice.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Deletion of the mouse myocardial Nppb gene alleviates sepsis-induced myocardial dysfunction.Journal of molecular histology · 2026Article
- miR‑223‑3p promotes microglial lactylation and M1 polarization via the FBXW7/Notch1/Hes1/SIRT1 axis.International journal of molecular medicine · 2026Article
- Endothelial Notch1 drives multicellular remodelling during hyaloid vessel regression.Angiogenesis · 2026Article
- Integrative analysis of bulk and single-nucleus transcriptomes suggests proteostasis- and metabolism-related alterations in the right ventricular outflow tract of non-syndromic Tetralogy of Fallot.Functional & integrative genomics · 2026Article
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Calcific aortic valve disease: can targeting endothelial-mesenchymal transition be a new alternative to surgery?-a narrative review.Cardiovascular diagnosis and therapy · 2026Review
- Review
- DNA methylation analysis of NOTCH1 variants reveals the first episignature for non-syndromic congenital heart defects.Genome medicine · 2026Article
- Cardiac EndMT and EpiMT as a developmental continuum: integration of mechanical, metabolic, and epigenetic regulation.Frontiers in cell and developmental biology · 2026Review
- CircIdh2 Attenuates Endothelial-to-Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential.Cardiovascular therapeutics · 2026Article
- Probiotics and Phytoantioxidants Target Coronary Endothelial Dysfunction in Irregular Sleep- and Obesity-Associated Cardiometabolic Syndrome.Life (Basel, Switzerland) · 2025Review
- Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025Review
- Mechanistic insights and emerging therapeutic strategies targeting endothelial dysfunction in cardiovascular diseases.Archives of pharmacal research · 2025Review
- Notch signaling pathway and heart development, congenital heart disease, and myocardial regeneration.Frontiers in bioengineering and biotechnology · 2025Review
- NOTCH1 and UPR signaling in embryonic heart development under maternal high-fat diet influence.Frontiers in medicine · 2025Article
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13 authors.
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Abstract
Notch signaling activation drives an endothelial-to-mesenchymal transition (EndMT) critical for heart development, although evidence suggests that the reprogramming of endothelial cell metabolism can regulate endothelial function independent of canonical cell signaling. Herein, we investigated the crosstalk between Notch signaling and metabolic reprogramming in the EndMT process. Biochemically, we find that the NOTCH1 intracellular domain (NICD1) localizes to endothelial cell mitochondria, where it interacts with and activates the complex to enhance mitochondrial metabolism. Targeting NICD1 to mitochondria induces more EndMT compared with wild-type NICD1, and small molecule activation of PDH during pregnancy improves the phenotype in a mouse model of congenital heart defect. A NOTCH1 mutation observed in non-syndromic tetralogy of Fallot patients decreases NICD1 mitochondrial localization and subsequent PDH activity in heart tissues. Altogether, our findings demonstrate NICD1 enrichment in mitochondria of the developing mouse heart, which induces EndMT by activating PDH and subsequently improving mitochondrial metabolism.
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