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

IF 3 4区医学 Q1 MEDICINE, GENERAL & INTERNAL

Archives of Medical Science Pub Date : 2024-01-12 eCollection Date: 2024-01-01 DOI:10.5114/aoms/177618

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

{"title":"Insulin-like growth factor-1 reduces cardiac autosis through decreasing AMPK/FOXO1 signaling and Na+/K+-ATPase-Beclin-1 interaction.","authors":"Katarina Banjac, Milan Obradovic, Sonja Zafirovic, Esma R Isenovic","doi":"10.5114/aoms/177618","DOIUrl":null,"url":null,"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.","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":"20 3","pages":"1011-1015"},"PeriodicalIF":3.0000,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11264057/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of Medical Science","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5114/aoms/177618","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}

引用次数: 0

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.

查看原文本刊更多论文

胰岛素样生长因子-1通过减少AMPK/FOXO1信号传导和Na+/K+-ATPase-Beclin-1相互作用减少心脏自律性。

引言胰岛素样生长因子-1（IGF-1）可促进心脏存活并抑制心脏自噬破坏：雄性Wistar大鼠接受IGF-1（50 µg/kg）治疗，注射24小时后切除心脏。方法：用IGF-1（50 µg/kg）治疗雄性Wistar大鼠，注射24小时后切除心脏，测定Beclin-1与钠/钾-腺苷三磷酸酶（Na+/K+-ATPase）α1亚基的相互作用水平，以及IGF-1受体/胰岛素受体（IGF-1R/IR）、叉头盒蛋白O1（FOXO1）和AMP激活蛋白激酶（AMPK）的磷酸化形式：结果表明，IGF-1能降低大鼠心脏中Beclin-1与Na+/K+-ATPase的结合（p < 0.05），增加IGF-1R/IR和FOXO1的磷酸化（p < 0.05），降低AMPK的磷酸化（p < 0.01）：结论：IGF-1新疗法可控制自体坏死，并将心肌细胞死亡率降至最低。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Archives of Medical Science 医学-医学：内科

CiteScore

4.90

自引率

7.90%

发文量

139

审稿时长

1.7 months

期刊介绍： Archives of Medical Science (AMS) publishes high quality original articles and reviews of recognized scientists that deal with all scientific medicine. AMS opens the possibilities for young, capable scientists. The journal would like to give them a chance to have a publication following matter-of-fact, professional review by outstanding, famous medical scientists. Thanks to that they will have an opportunity to present their study results and/or receive useful advice about the mistakes they have made so far. The second equally important aim is a presentation of review manuscripts of recognized scientists about the educational capacity, in order that young scientists, often at the beginning of their scientific carrier, could constantly deepen their medical knowledge and be up-to-date with current guidelines and trends in world-wide medicine. The fact that our educational articles are written by world-famous scientists determines their innovation and the highest quality.