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在糖尿病动脉样硬化中,ETV5介导的DDIT4的转录抑制阻断了巨细胞的前炎性活化

Lili Shi¹, Tingting Sun¹, Di Huo¹

¹Department of Cadre Ward, The First Affiliated Hospital of Harbin Medical University, No. 23, Postal Street, Harbin, 150001, Heilongjiang, PR China.

Cardiovascular toxicology

|January 26, 2025

概括

糖尿病通过促进巨细胞炎症增加动脉样硬化风险. 失去ETV5维持DDIT4转录,驱动这种炎症反应并恶化糖尿病动脉样硬化.

科学领域:

心血管生物学心血管生物学
免疫学免疫学免疫学
代谢性疾病研究研究

背景情况:

糖尿病患者表现出动脉样硬化风险增加,但涉及巨细胞激活的精确机制仍然不完全理解.
巨细胞在动脉样硬化发展背后的炎症过程中发挥着至关重要的作用.

研究的目的:

阐明连接糖尿病的分子机制,巨细胞的前炎性激活,以及动脉样硬化的进展.
研究DDIT4及其调节器ETV5在糖尿病动脉样硬化中的作用.

主要方法:

来自患者和糖尿病小鼠模型的巨细胞转录组的生物信息分析.
产生和分析DDIT4缺乏的LDLR-/-小鼠,吃西方饮食.
在动脉样硬化病变中评估巨细胞标记物,斑块特征和细胞含量.

主要成果:

在糖尿病动脉样硬化中,DDIT4的表达上调. 在小鼠中,DDIT4缺乏减少了巨细胞的炎症因子,死亡区域,并提高了斑块的稳定性.
ETV5调节了DDIT4表达;ETV5倒置加剧了前炎性巨细胞反应和降低了斑块稳定性,DDIT4倒置扭转了效应.

结论:

失去ETV5通过维持DDIT4转录来促进糖尿病动脉样硬化,从而导致促炎性巨细胞激活.
DDIT4被确定为糖尿病动脉样硬化发展的关键调解剂,提供潜在的治疗点.

关键词:

在DDIT4中,DDIT4是DDIT4.糖尿病动脉样硬化糖尿病动脉样硬化在 ETV5 上播放.巨细胞是一个巨细胞.斑块的稳定性斑块的稳定性

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