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CARDIOLOGY / RESEARCH LETTER
Insulin-like growth factor-1 reduces cardiac autosis through decreasing AMPK/FOXO1 signaling and Na+/K+-ATPase-Beclin-1 interaction
1
Department of Radiobiology and Molecular Genetics, “VINČA” Institute of Nuclear Sciences – National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia
These authors had equal contribution to this work
Submission date: 2023-10-12
Final revision date: 2023-12-09
Acceptance date: 2023-12-26
Online publication date: 2024-01-12
Corresponding author
MIlan Obradovic
Department of Radiobiology and Molecular Genetics, “VINČA” Institute of Nuclear Sciences – National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia
Department of Radiobiology and Molecular Genetics, “VINČA” Institute of Nuclear Sciences – National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia
Arch Med Sci 2024;20(3):1011-1015
KEYWORDS
TOPICS
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.
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.
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| eISSN: | 1896-9151 |
| ISSN: | 1734-1922 |
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