Insulin-like growth factor-1 reduces cardiac autosis through decreasing AMPK/FOXO1 signaling and Na+/K+-ATPase-Beclin-1 interaction

Abstract

Introduction Insulin-like growth factor-1 (IGF-1) promotes survival and inhibits cardiac autophagy disruption. Methods Male Wistar rats were treated with IGF-1 (50 µg/kg), and 24 h after injection hearts were excised. The level of interaction between Beclin-1 and the α 1 subunit of sodium/potassium-adenosine triphosphates (Na + /K + -ATPase), and phosphorylated forms of IGF-1 receptor/insulin receptor (IGF-1R/IR), forkhead box protein O1 (FOXO1) and AMP-activated protein kinase (AMPK) were measured. Results The results indicate that IGF-1 decreased Beclin-1’s association with Na + /K + -ATPase ( p < 0.05), increased IGF-1R/IR and FOXO1 phosphorylation ( p < 0.05), and decreased AMPK phosphorylation ( p < 0.01) in rats’ hearts. Conclusions The new IGF-1 therapy may control autosis and minimize cardiomyocyte mortality.

Keywords

• na + /k + -atpase
• association of na + /k + -atpase and beclin-1
• cardiac autosis
• ampk
• foxo1