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ATP5me可以缓解高葡萄糖诱导的心肌细胞损伤

Qingsha Hou¹, Fang Yan¹, Xiuling Li¹

¹Obstetrical Department, the First People's Hospital of Yunnan Province, the Affiliated Hospital of Kunming University of Science and Technology, No.157 Jinbi Road, Kunming, Yunnan, 650032, China.

International immunopharmacology

|February 6, 2024

概括

孕期糖尿病 (GDM) 在母亲可能会损害胎儿的心脏发育. 这项研究发现,ATP合成酶膜子单元E (ATP5me) 能够防止这种损伤,从而成为潜在的治疗点.

科学领域:

心血管生物学心血管生物学
发育生物学发展生物学
代谢障碍代谢障碍代谢障碍

背景情况:

孕期糖尿病 (GDM) 与胎儿心肌重塑和心脏功能受损有关.
由GDM引起的胎儿心脏损伤的精确分子路径尚未完全理解.
RNA测序 (RNA-seq) 可以识别GDM对胎儿心脏的影响中的关键分子参与者.

研究的目的:

为了研究1型GDM诱导的胎儿心肌损伤的分子机制.
在发育中的胎儿心脏中识别受GDM影响的特定基因和通路.
探索ATP合成酶膜子单元E (ATP5me) 在缓解GDM相关心脏损伤中的作用.

主要方法:

开发了一种1型GDM大鼠模型,使用链毒素 (STZ).
评估了母亲和后代的生理参数,心脏损伤标志物和氧化应激.
利用RNA-seq识别GDM后代心中的差异表达mRNA.
在高葡萄糖暴露的H9C2细胞中评估了细胞反应 (增殖,亡,氧化应激) 和调节的ATP5me水平.

主要成果:

在GDM小鼠中,母体和胎儿体重降低,葡萄糖耐受性受损.
在GDM后代的心脏中,心肌损伤 (CK-MB,cTnT,hs-CRP) 和氧化应激 (ROS,MDA) 的标志物升高,SOD降低.
RNA-seq揭示了GDM心脏中462个差异表达的mRNA,主要涉及免疫力,氧化还原反应和细胞通信.
在GDM后代心脏和高葡萄糖体内ATP5me表达减少;过度表达ATP5me保护H9C2细胞免受高葡萄糖诱导的损伤.

结论:

ATP5me对1型GDM诱导的胎儿心肌损伤起着保护作用.
减少ATP5me表达是GDM对胎儿心脏影响的潜在分子机制.
向ATP5me可能为与GDM相关的胎儿心脏并发症提供一种新的治疗策略.

关键词:

在ATP合成酶膜子单元EE中.孕期糖尿病是一种糖尿病.心肌损伤是指心肌损伤.他们有后代,有后代的后代.氧化应激是一种氧化应激.

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