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MTERF1通过AMPK/mTOR通路调节糖尿病脏病中的足细胞线粒体DNA复制障碍和线粒体功能障碍

Haiying Tao¹, Ling'an Yu²

¹Department of Endocrinology, Taizhou First People's Hospital, Taizhou, Zhejiang, China.

Annals of clinical and laboratory science

|November 18, 2025

概括

线粒体转录终止因子1 (MTERF1) 在糖尿病病中保护细胞免受高葡萄糖损伤. 过度表达MTERF1激活AMPK/mTOR通路,改善线粒体功能和DNA复制.

科学领域:

细胞生物学细胞生物学
分子生物学分子生物学
腎臟病學 (nephrology) 是一種醫學專業.

背景情况:

糖尿病脏病 (DN) 涉及皮质细胞损伤和线粒体功能障碍.
线粒体转录终结因子1 (MTERF1) 在线粒体DNA (mtDNA) 调节中起作用.
在DN podocytes中MTERF1的确切机制尚不清楚.

研究的目的:

阐明MTERF1在调节mtDNA复制和糖尿病脏病中 podocyte 线粒体功能的作用.
研究涉及AMPK/mTOR信号通路的潜在分子机制.

主要方法:

已建立的链毒素诱导型I型糖尿病小鼠模型和高葡萄糖 (HG) 治疗的MPC-5 podocyte细胞模型.
在体内评估功能,球损伤和MTERF1表达.
量化细胞亡,活力,mtDNA拷贝数,ATP生产,线粒体活性氧物种 (mtROS) 和线粒体膜潜力 (MMP) 在体外.
利用MTERF1过度表达细胞和AMPK抑制剂 (化合物C) 来探索通路激活.

主要成果:

DN小鼠表现出高血糖,功能障碍,球膜损伤和MTERF1表达的降低.
用HG治疗的细胞表现出亡的增加,活力的降低,MTERF1,mtDNA拷贝数和ATP水平的降低.
在HG podocytes中MTERF1过度表达恢复了mtDNA复制,ATP生产,线粒体膜潜力,并激活了AMPK/mTOR通路,同时减少了mtROS.
抑制AMPK/mTOR信号反转了MTERF1.1的保护作用.

结论:

过度表达MTERF1通过增强mtDNA复制和线粒体功能来减轻高葡萄糖诱导的细胞损伤.
激活AMPK/mTOR信号通路对于MTERF1在糖尿病病中的保护作用至关重要.
MTERF1代表了改善DNA中线粒体健康的潜在治疗标.

关键词:

在AMPK/mTOR信号通路中.在MTERF1中,MTERF1是MTERF1.糖尿病性脏病糖尿病性脏病线粒体功能障碍线粒体功能障碍

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