胰岛素样生长因子-1通过降低AMPK/FOXO1信号通路以及Na/K-ATP酶与Beclin-1的相互作用来减少心脏自噬。
Insulin-like growth factor-1 reduces cardiac autosis through decreasing AMPK/FOXO1 signaling and Na/K-ATPase-Beclin-1 interaction.
作者信息
Banjac Katarina, Obradovic Milan, Zafirovic Sonja, Isenovic Esma R
机构信息
Department of Radiobiology and Molecular Genetics, "VINČA" Institute of Nuclear Sciences - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.
出版信息
Arch Med Sci. 2024 Jan 12;20(3):1011-1015. doi: 10.5114/aoms/177618. eCollection 2024.
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.
引言
胰岛素样生长因子-1（IGF-1）可促进存活并抑制心脏自噬破坏。
方法
用IGF-1（50μg/kg）处理雄性Wistar大鼠，注射后24小时取出心脏。检测Beclin-1与钠/钾-三磷酸腺苷酶（Na/K-ATPase）α亚基之间的相互作用水平，以及IGF-1受体/胰岛素受体（IGF-1R/IR）、叉头框蛋白O1（FOXO1）和AMP活化蛋白激酶（AMPK）的磷酸化形式。
结果
结果表明，IGF-1降低了大鼠心脏中Beclin-1与Na/K-ATPase的结合（<0.05），增加了IGF-1R/IR和FOXO1的磷酸化（<0.05），并降低了AMPK的磷酸化（<0.01）。
结论
新的IGF-1疗法可能控制自噬并使心肌细胞死亡率降至最低。
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