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Cardiac-specific beta-catenin deletion dysregulates energetic metabolism and mitochondrial function in perinatal cardiomyocytes

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Winata,  Cecilia L.
Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Citation

Balatskyi, V. V., Vaskivskyi, V. O., Myronova, A., Avramets, D., Abu Nahia, K., Macewicz, L. L., et al. (2021). Cardiac-specific beta-catenin deletion dysregulates energetic metabolism and mitochondrial function in perinatal cardiomyocytes. MITOCHONDRION, 60, 59-69. doi:10.1016/j.mito.2021.07.005.


Cite as: http://hdl.handle.net/21.11116/0000-0009-6A37-3
Abstract
beta-Catenin signaling pathway regulates cardiomyocytes proliferation and differentiation, though its involvement in metabolic regulation of cardiomyocytes remains unknown. We used one-day-old mice with cardiac-specific knockout of beta-catenin and neonatal rat ventricular myocytes treated with beta-catenin inhibitor to investigate the role of beta-catenin metabolism regulation in perinatal cardiomyocytes. Transcriptomics of perinatal beta-cateninablated hearts revealed a dramatic shift in the expression of genes involved in metabolic processes. Further analysis indicated an inhibition of lipolysis and glycolysis in both in vitro and in vivo models. Finally, we showed that beta-catenin deficiency leads to mitochondria dysfunction via the downregulation of Sirt1/PGC-1 alpha pathway. We conclude that cardiac-specific beta-catenin ablation disrupts the energy substrate shift that is essential for postnatal heart maturation, leading to perinatal lethality of homozygous beta-catenin knockout mice.