TRIIODOTHYRONINE (T3) IMPROVES POST-ISCHEMIC MECHANICAL RECOVERY AND MITOCHONDRIAL FUNCTION PRESERVATION BY ENHANCING AMP-ACTIVATED PROTEIN KINASE (AMPK) ACTIVATION.

FERNANDEZ PAZOS, MARIA DE LAS MERCEDES; MESTRE CORDERO, VICTORIA; MARINA PRENDES, MARIA GABRIELA; CORDOBA, MAILEN FLORENCIA; VELEZ, DEBORA; HERMANN, ROMINA; REZNIK, FEDERICO JOAQUIN; FELLET, ANDREA

Ciudad Autónoma de Buenos Aires

Congreso; REUNIÓN DE SOCIEDADES DE BIOCIENCIAS 2020; 2020

SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA (SAIC), SOCIEDAD ARGENTINA DE FISIOLOGÍA (SAFIS), SOCIEDAD ARGENTINA DE INMUNOLOGÍA (SAI)

Experimental evidence has shown that T3 can regulate cardioprotectivesignaling pathways, increasing myocardium resistance toischemia-reperfusion injury. Although novel studies have suggestedthat T3 enhances the activation of AMPK, a key enzyme regulator ofenergy balance, its role has not been elucidated yet.In the present study the role of AMPK in the effects exerted by acutetreatment with T3 on ischemic-reperfused myocardium was investigated.For this aim, rat left atria were subjected to 75 min simulatedischemia (I)-75 min reperfusion (R), in the presence of T3 (60 nM)and AMPK inhibitor, Compound C (CC; 10 μM). ANOVA, followed byTukey, n=8/group.Results showed that CC prevented the increase of AMPK activationinduced by T3 (End stabilization period (ESP):1.33±0.02,I-R:2.20±0.11*, I-R+T3:2.79±0.10*#, I-R+T3+CC:1.17±0.10AU;*p