@article {119,
	title = {Cardiac-specific β-catenin deletion dysregulates energetic metabolism and mitochondrial function in perinatal cardiomyocytes.},
	journal = {Mitochondrion},
	volume = {60},
	year = {2021},
	month = {2021 09},
	pages = {59-69},
	abstract = {<p>β-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 β-catenin and neonatal rat ventricular myocytes treated with β-catenin inhibitor to investigate the role of β-catenin metabolism regulation in perinatal cardiomyocytes. Transcriptomics of perinatal β-catenin-ablated 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 β-catenin deficiency leads to mitochondria dysfunction via the downregulation of Sirt1/PGC-1α pathway. We conclude that cardiac-specific β-catenin ablation disrupts the energy substrate shift that is essential for postnatal heart maturation, leading to perinatal lethality of homozygous β-catenin knockout mice.</p>},
	issn = {1872-8278},
	doi = {10.1016/j.mito.2021.07.005},
	author = {Balatskyi, Volodymyr V and Vaskivskyi, Vasyl O and Myronova, Anna and Avramets, Diana and Nahia, Karim Abu and Macewicz, Larysa L and Ruban, Tetiana P and Kucherenko, Dar{\textquoteright}ya Yu and Soldatkin, Oleksandr O and Lushnikova, Iryna V and Skibo, Galyna G and Winata, Cecilia L and Dobrzyn, Pawel and Piven, Oksana O}
}
