Error message

User warning: The following module is missing from the file system: recaptcha. For information about how to fix this, see the documentation page. in _drupal_trigger_error_with_delayed_logging() (line 1156 of /home/lpryszcz/Public/zdg_lab_site/includes/bootstrap.inc).

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

TitleCardiac-specific β-catenin deletion dysregulates energetic metabolism and mitochondrial function in perinatal cardiomyocytes.
Publication TypeJournal Article
Year of Publication2021
AuthorsBalatskyi, VV, Vaskivskyi, VO, Myronova, A, Avramets, D, Nahia, KAbu, Macewicz, LL, Ruban, TP, Kucherenko, D'yaYu, Soldatkin, OO, Lushnikova, IV, Skibo, GG, Winata, CL, Dobrzyn, P, Piven, OO
JournalMitochondrion
Volume60
Pagination59-69
Date Published2021 09
ISSN1872-8278
Abstract

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.

DOI10.1016/j.mito.2021.07.005
Alternate JournalMitochondrion
Citation Key119
PubMed ID34303005