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通过FBXO45介导的GPX4无处不在,SETD7驱动糖尿病内皮功能障碍

Wen Zhong¹, Ruoxue Chen¹, Jialin Zhao¹

¹Phenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital, Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, 825, Zhangheng Road, Pudong New District, Shanghai, 201203, China.

Cardiovascular diabetology

|April 24, 2025

概括

糖尿病内皮功能障碍由SETD7恶化,它促进氧化应激和脂质过氧化. 抑制SETD7部分恢复了血管功能,并减少了高血糖引起的损伤.

科学领域:

内分泌学在内分泌学.
分子生物学分子生物学
心血管研究研究心血管研究

背景情况:

糖尿病血管病是主要的并发症,内皮损伤有助于器官功能障碍.
在糖尿病内皮功能障碍中SETD7 (基因组甲基转移酶) 的作用尚不清楚.
这项研究研究了SETD7在高葡萄糖诱导的内皮损伤中的机制.

研究的目的:

阐明SETD7在糖尿病内皮功能障碍中的参与和潜在机制.
研究SETD7对高血糖引起的血管损伤的影响.
评估SETD7对内皮细胞中氧化应激和脂质过氧化的调节.

主要方法:

在db/db小鼠中通过AAV利用了SETD7淘汰赛小鼠和内皮特异性SETD7中断.
评估了对斯特雷普托佐托辛 (STZ) 诱导的高血糖和血管损伤的影响.
在高葡萄糖条件下对大鼠主动动脉内皮细胞 (RAEC) 进行了体外研究,操纵了SETD7.

主要成果:

在糖尿病小鼠模型中,SETD7缺乏部分恢复了血管功能,并减少了炎症.
通过Glutathione Peroxidase 4 (GPX4) 介导的脂质过氧化,SETD7激活加剧了氧化应激和内皮功能障碍.
由于SETD7缺乏,减少了p53单甲基化,阻断了FBXO45转录,抑制了GPX4降解.

结论:

SETD7-p53-FBXO45-GPX4通路与高葡萄糖诱导的氧化应激和内皮功能障碍有关.
针对这种途径可以减轻高血糖引起的内皮损伤.
研究结果强调SETD7是糖尿病血管并发症的潜在治疗点.

关键词:

糖尿病内皮功能障碍糖尿病内皮功能障碍在FBXO45中,FBXO45是什么?在GPX4中使用GPX4.脂质过氧化过氧化在SETD7中,SETD7是SETD7.在p53中,p53是什么?

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