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

Katarina Banjac; Milan Obradovic; Sonja Zafirovic; Esma R Isenovic

doi:10.5114/aoms/177618

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

Arch Med Sci. 2024 Jan 12;20(3):1011-1015. doi: 10.5114/aoms/177618. eCollection 2024.

Authors

Katarina Banjac¹, Milan Obradovic¹, Sonja Zafirovic¹, Esma R Isenovic¹

Affiliation

¹ Department of Radiobiology and Molecular Genetics, "VINČA" Institute of Nuclear Sciences - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.

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 α₁ 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: AMPK; FOXO1; Na+/K+-ATPase; association of Na+/K+-ATPase and Beclin-1; cardiac autosis.

Grants and funding

Funding This work was funded by the Ministry of Science, Technological Development and Innovation of the Republic of Serbia (Contract No#451-03-47/2023-01/200017).