MTORC1 Regulates the Metabolic Switch of Postnatal Cardiomyocytes During Regeneration.

ABSTRACT: The metabolic switch from glycolysis to fatty acid oxidation in postnatal cardiomyocytes contributes to the loss of the cardiac regenerative potential of the mammalian heart. However, the mechanisms that regulate this metabolic switch remain unclear. The protein kinase complex mechanistic target of rapamycin complex 1 (mTORC1) is a central signaling hub that regulates cellular metabolism and protein synthesis, yet its role during mammalian heart regeneration and postnatal metabolic maturation is undefined. Here, we use immunoblotting, rapamycin treatment, myocardial infarction, and global proteomics to define the role of mTORC1 in postnatal heart development and regeneration. Our results demonstrate that the activity of mTORC1 is dynamically regulated between the regenerating and the non-r

SUBMITTER: Paltzer WG 

PROVIDER: S-EPMC10515815 | biostudies-literature | 2023 Sep

REPOSITORIES: biostudies-literature