Activation of amino acid metabolic program in cardiac HIF1-alpha-deficient mice
Ivan Menendez-Montes, Beatriz Escobar, Manuel J. Gómez, Teresa Albendea-Gomez, Beatriz Palacios, Elena Bonzón‐Kulichenko, José Luis Izquierdo-García, Ana Vanessa Alonso, Alessia Ferrarini, Luis Jesús Jiménez‐Borreguero, Jesús Ruı́z-Cabello, Jesús Vázquez, Silvia Martı́n-Puig
Abstract
mutants display normal fatty acid oxidation program and do not show cardiac dysfunction in the adulthood. Our results demonstrate that cardiac HIF1 signaling and glycolysis are dispensable for mouse heart development and reveal the metabolic flexibility of the embryonic myocardium to consume amino acids, raising the potential use of alternative metabolic substrates as therapeutic interventions during ischemic events.
Topics & Concepts
GlycolysisHIF1AAnaerobic glycolysisCatabolismBeta oxidationCell biologyEmbryonic stem cellDownregulation and upregulationMitochondrionAlpha (finance)Alpha ketoglutarateBiologyAmino acidMetabolic pathwaySerineBiochemistryChemistryMetabolismMedicineGeneEnzymeConstruct validityPatient satisfactionNursingPhosphorylationRNA modifications and cancerCongenital heart defects researchMitochondrial Function and Pathology