Artículo de revista
Alteration in mitochondrial Ca2+ uptake disrupts insulin signaling in hypertrophic cardiomyocytes
Cell Communication and Signaling, Volumen 12, Issue 1, 2018,
Contreras Ferrat, Ariel Eduardo
Vásquez Trincado, César Alonso
Morales, Pablo E.
López Crisosto, Camila
Sotomayor Flores, Cristian Alejandro
Chiong Lay, Mario
Rothermel, Beverly A.
Lavandero González, Sergio
© 2014 Gutierrez et al.; licensee BioMed Central Ltd. Background: Cardiac hypertrophy is characterized by alterations in both cardiac bioenergetics and insulin sensitivity. Insulin promotes glucose uptake by cardiomyocytes and its use as a substrate for glycolysis and mitochondrial oxidation in order to maintain the high cardiac energy demands. Insulin stimulates Ca2+ release from the endoplasmic reticulum, however, how this translates to changes in mitochondrial metabolism in either healthy or hypertrophic cardiomyocytes is not fully understood. Results: In the present study we investigated insulin-dependent mitochondrial Ca2+ signaling in normal and norepinephrine or insulin like growth factor-1-induced hypertrophic cardiomyocytes. Using mitochondrion-selective Ca2+-fluorescent probes we showed that insulin increases mitochondrial Ca2+ levels. This signal was inhibited by the pharmacological blockade of either the inositol 1,4,5-triphosphate receptor or the mitochondrial Ca2+ uniport