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

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 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 ( < 0.05), increased IGF-1R/IR and FOXO1 phosphorylation ( < 0.05), and decreased AMPK phosphorylation ( < 0.01) in rats' hearts.

Conclusions: The new IGF-1 therapy may control autosis and minimize cardiomyocyte mortality.