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Hermann R, Mestre Cordero VE, Fernández Pazos MLM, et al. Role of AMPK in the protective effects exerted by triiodothyronine in ischemic-reperfused myocardium. J Mol Endocrinol. 2021;66(3):207-221doi: 10.1530/JME-20-0314.
Hermann, R., Mestre Cordero, V. E., Fernández Pazos, M. L. M., Córdoba, M. F., Reznik, F. J., Vélez, D. E., Fellet, A. L., & Marina Prendes, M. G. (2021). Role of AMPK in the protective effects exerted by triiodothyronine in ischemic-reperfused myocardium. Journal of molecular endocrinology, 66(3), 207-221. https://doi.org/10.1530/JME-20-0314
Hermann, Romina, et al. "Role of AMPK in the protective effects exerted by triiodothyronine in ischemic-reperfused myocardium." Journal of molecular endocrinology vol. 66,3 (2021): 207-221. doi: https://doi.org/10.1530/JME-20-0314
Hermann R, Mestre Cordero VE, Fernández Pazos MLM, Córdoba MF, Reznik FJ, Vélez DE, Fellet AL, Marina Prendes MG. Role of AMPK in the protective effects exerted by triiodothyronine in ischemic-reperfused myocardium. J Mol Endocrinol. 2021 Mar;66(3):207-221. doi: 10.1530/JME-20-0314. PMID: 33640872.
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J Mol Endocrinol. 2021 Mar;66(3):207-221. doi: 10.1530/JME-20-0314.

Role of AMPK in the protective effects exerted by triiodothyronine in ischemic-reperfused myocardium.

Journal of molecular endocrinology

Romina Hermann, Victoria Evangelina Mestre Cordero, María de Las Mercedes Fernández Pazos, Mailen Florencia Córdoba, Federico Joaquín Reznik, Débora Elisabet Vélez, Andrea Lorena Fellet, María Gabriela Marina Prendes

Affiliations

  1. Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Ciencias Biológicas, Cátedra de Fisiología, Buenos Aires, Argentina.
  2. CONICET - Universidad de Buenos Aires, Instituto de Química y Metabolismo del Fármaco (IQUIMEFA), Buenos Aires, Argentina.

PMID: 33640872 DOI: 10.1530/JME-20-0314

Abstract

Recent studies have provided evidence that triiodothyronine (T3) might play an effective role in the recovery of ischemic myocardium, through the preservation of mitochondrial function and the improvement of energy substrate metabolism. To this respect, it has been suggested that T3 could activate AMP-activated protein kinase (AMPK), the cellular 'fuel-gauge' enzyme, although its role has yet to be elucidated. The aim of the present study was to investigate the effects produced by acute treatment with T3 (60 nM) and the pharmacological inhibition of AMPK by compound C on isolated rat left atria subjected to 75 min simulated ischemia-75 min reperfusion. Results showed that T3 increased AMPK activation during simulated ischemia-reperfusion, while compound C prevented it. At the end of simulated reperfusion, acute T3 treatment increased contractile function recovery and cellular viability conservation. Mitochondrial ultrastructure was better preserved in the presence of T3 as well as mitochondrial ATP production rate and tissue ATP content. Calcium retention capacity, a parameter widely used as an indicator of the resistance of mitochondrial permeability transition pore (MPTP) to opening, and GSK-3β phosphorylation, a master switch enzyme that limits MPTP opening, were increased by T3 administration. All these beneficial effects exerted by T3 acute treatment were prevented when compound C was co-administrated. The present study provided original evidence that T3 enhances intrinsic activation of AMPK during myocardial ischemia-reperfusion, being this enzyme involved, at least in part, in the protective effects exerted by T3, contributing to mitochondrial structure and function preservation, post-ischemic contractile recovery and conservation of cellular viability.

Keywords: AMP-activated protein kinase; cardiprotection; compound C; myocardium; simulated ischemia-reperfusion; triiodothyronine

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