Análise do papel da proteína quinase ativada pela AMP (AMPK) na hipertrofia do cardiomiócito induzida pelo hormônio tiroideano.

Abstract

Previous studies of literature, including our laboratory results have shown that high levels of thyroid hormones (TH) induce significant cardiac hypertrophy, observed both in vivo and in vitro experiments. Recently, some studies have shown that TH are also able to rapidly modulate the phosphorylation state of protein kinases related to cardiac hypertrophy process by non-genomic actions. In this sense, experimental evidences indicate that AMP-activated protein kinase (AMPK) is an important target in the control of hypertrophic growth, since the activation of this enzyme determines wide variety of physiological effects, including the control of enzymes related to protein synthesis. Thus, the objectives of this study were to evaluate the effects of TH on the modulation of AMPK signaling pathway and to check the possible involvement of this kinase in vitro model of hypertrophy induced by TH. The results showed that this hormone rapidly activates AMPK and related proteins to this signaling. Furthermore, pharmacological stimulation of AMPK attenuated cardiomyocyte hypertrophy induced by TH. These data suggest that AMPK is a possible and interesting therapeutic tool in cardiovascular disease such as cardiac hypertrophy.

Avaliação Das Atitudes De Segurança Da Equipe De Enfermagem Da Atenção Básica

“…A metformina inibe a cadeia de transporte de elétrons e síntese de Adenosina Trifosfato (SANTOMAURO JÚNIOR et al, 2008). Além disso, ela regula a proteína quinase ativada por Adenina Monofosfato (AMP) (AMPK) e o alvo mecanicista da rapamicina complexo 1 (mtorc1) por múltiplos mecanismos não-exclusivos mutuamente (TAKANO, 2011).…”