Congenital heart defects research

The paper analyzes transcriptomic and chromatin accessibility changes in zebrafish cardiomyocytes during heart development to identify key regulatory networks and their disruption in mutant lines.

This study shows that PIEZO1 is essential for outflow tract and aortic valve development in zebrafish and identifies PIEZO1 variants linked to bicuspid aortic valve in humans.

The paper shows Myc is not essential for cardiac development in mice but can replace Mycn function in its absence through cell competition.

This study shows that Nrp1 is essential for zebrafish heart regeneration by enabling epicardial activation, migration, and revascularization after injury.

The paper shows Pax9 is essential for cardiovascular development and interacts with Tbx1 in the pharyngeal endoderm to regulate 4th pharyngeal arch artery formation.

This study shows that deleting NOTCH-RBPJ in the myocardium does not impair heart development or function, but deleting it in both myocardial and endocardial progenitors causes cardiac defects.

The paper uses single-cell RNA-seq and ATAC-seq to study cardiac progenitor cell fate transitions, identifying roles for Isl1 and Nkx2-5 in lineage commitment and gene regulatory networks.

This study shows that loss of embryonic neural crest cardiomyocytes in zebrafish leads to adult hypertrophic cardiomyopathy with altered heart structure and function.

This study provides a molecular atlas of postnatal mouse heart development by integrating transcriptomics, proteomics, and metabolomics data to identify metabolism-related mechanisms linked to the loss of cardiac regeneration.

The paper tests a human PBX3 variant in zebrafish to show it may modify congenital heart defect risk by enhancing cardiac morphogenesis defects.

The paper shows that culturing adult cardiac stem cells reduces transcriptome variability and alters gene expression, potentially affecting their therapeutic efficacy.

This study tracks zebrafish heart development and shows that the ventricle forms continuously from progenitor cells, with FGF signaling playing a critical role in this process.

The paper investigates fibrosis resolution in regenerating zebrafish hearts, finding that fibroblasts become inactivated rather than being eliminated, and that fibrosis supports cardiomyocyte proliferation.

The paper screens for DICER1 mutations in TGA patients and finds no apparent pathological mutations.

The paper uses live imaging of mouse embryos to show that heart tube development involves alternating phases of cardiac differentiation and morphogenesis.

The paper generates two new zebrafish tbx5a frameshift alleles and compares their phenotypes to the classic hst mutant, finding differences in heart defects.

This study shows that Baf60c regulates gene expression programs critical for heart development and function by interacting with Myocardin and controlling contractile proteins and metabolic genes.