Integrated Proteomics Identifies Troponin I Isoform Switch as a Regulator of a Sarcomere-Metabolism Axis During Cardiac Regeneration.

ABSTRACT: Adult mammalian cardiomyocytes have limited proliferative potential, and after myocardial infarction (MI), injured cardiac tissue is replaced with fibrotic scar rather than with functioning myocardium. In contrast, the neonatal mouse heart possesses a regenerative capacity governed by cardiomyocyte proliferation; however, a metabolic switch from glycolysis to fatty acid oxidation during postnatal development results in loss of this regenerative capacity. Interestingly, a sarcomere isoform switch also takes place during postnatal development where slow skeletal troponin I (ssTnI) is replaced with cardiac troponin I (cTnI). In this study, we first employ integrated quantitative bottom-up and top-down proteomics to comprehensively define the proteomic and sarcomeric landscape during postnatal

SUBMITTER: Aballo TJ 

PROVIDER: S-EPMC10634731 | biostudies-literature | 2023 Oct

REPOSITORIES: biostudies-literature