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    Area of Science:

    • Cardiovascular Biology
    • Mitochondrial Metabolism
    • Developmental Biology

    Background:

    • Cardiac morphogenesis requires coordinated metabolic and structural maturation.
    • The mitochondrial citrate carrier (SLC25A1) was previously identified as a key regulator of embryonic heart development.

    Purpose of the Study:

    • To investigate the cell-autonomous role of SLC25A1 in cardiomyocyte differentiation, mitochondrial maturation, and ventricular morphogenesis.
    • To elucidate the molecular mechanisms linking SLC25A1 function to cardiac development.

    Main Methods:

    • Systemic and cardiomyocyte-specific Slc25a1 deletion in mice.
    • SLC25A1 knockout (KO) in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs).
    • Transcriptomic analysis of SLC25A1-deficient hearts.
    • In vivo and in vitro assessments of cardiomyocyte function and mitochondrial health.

    Main Results:

    • SLC25A1 loss impairs cardiomyocyte differentiation, mitochondrial function, and myofibril organization.
    • Defective ventricular wall compaction observed in vivo.
    • Transcriptomic analysis revealed dysregulated gene programs related to cardiomyocyte differentiation and mitochondrial function.

    Conclusions:

    • SLC25A1 acts cell-autonomously within cardiomyocytes to regulate cardiac development.
    • SLC25A1 links mitochondrial citrate export to developmental gene programs.
    • A mitochondrial regulatory axis involving SLC25A1 is critical for cardiomyocyte maturation and cardiac morphogenesis, offering insights into congenital heart disease.