Paul T. Mungai

Aug 7, 2024 | digitalcommons.library.tmc.edu | Gregory B. Waypa |Kimberly Smith |Paul T. Mungai |Vincent J. Dudley

AbstractNewborn mammalian cardiomyocytes quickly transition from a fetal to an adult phenotype that utilizes mitochondrial oxidative phosphorylation but loses mitotic capacity. We tested whether forced reversal of adult cardiomyocytes back to a fetal glycolytic phenotype would restore proliferative capacity. We deleted Uqcrfs1 (mitochondrial Rieske iron-sulfur protein, RISP) in hearts of adult mice. As RISP protein decreased, heart mitochondrial function declined, and glucose utilization increased.

May 9, 2024 | jci.org | Gregory B. Waypa |Kimberly Smith |Paul T. Mungai |Vincent J. Dudley

ResearchCardiologyMetabolismOpen Access | 10.1172/JCI165482 J Clin Invest. https://doi.org/10.1172/JCI165482. Copyright © 2024, Waypa et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.