ArticleNature communications2025
Single-nuclei multiomics analysis identifies abnormal cardiomyocytes in a murine model of cardiac development.
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 7 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Spatially resolved single cell atlas deciphers SAA1 inflammatory epithelial cells.International journal of oral science · 2026Article
- The dual-enhanced graph learning framework DePass allows paired data integration in single-cell and spatial multiomics.Nature cell biology · 2026Article
- Protocol for isolation of nuclei from murine cardiac tissue for single-nucleus multiomic sequencing.STAR protocols · 2026Article
- Life-span-dependent transcriptional dynamics of the human heart.Science advances · 2026Article
- A miR-200b-Filamin A axis drives epicardial contribution to cardiogenesis.Scientific reports · 2026Article
- Activation of developmental transcription factors using RNA technology promotes heart repair.bioRxiv : the preprint server for biology · 2026Article
- Decoding cardiac metabolic reprogramming through single-cell multi-omics: from mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Transcription factors such as Tbx5, Gata4, Mef2c and Pitx2 are required during cardiac development, and in adult cardiac homeostasis. We demonstrate that the gene dosage and modulation of these factors are mediated in vivo by the miR-200 family. Inhibition of a single miR-200 family member within the cluster results in defects of the left ventricle and cardiomyocyte maturation during development. Inhibition of the entire miR-200 family results in a ventricular septal defect and embryonic lethality by embryonic day (E)16.5. Inhibition of each miR-200 family has distinct heart phenotypes in cell specific differentiation and maturation. snRNA-sequencing reveals an immature cardiomyocyte cell state, suggesting reduced differentiation of these cells. The miR-200 family members are critical regulators of early cardiac development through maintaining cardiomyocyte differentiation and maturation. In this report, we identify several transcription factors regulated by miR-200 during heart development, a role for miR-200 in specific heart defects, and an abnormal cardiomyocyte population.
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Registered trials
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