乳二烯通过调节巨细胞AMPK/mTOR信号依赖的自细胞来影响动脉样硬化进展
Bing Xia1, Jingwei Liang2, Yanlin Lu2
1School of Forensic Medicine, Guizhou Medical University, Guiyang, 550004, Guizhou, China. 372732293@qq.com.
Scientific reports
|March 28, 2025
概括
乳酸 (LTF) 可能通过促进AMPK/mTOR途径来帮助减少动脉样硬化 (AS),这表明它作为AS进展的预测标记物的潜力.
科学领域:
- 心血管生物学 心血管生物学
- 分子医学是分子医学.
- 病理学 病理学 病理学
背景情况:
- 动脉样硬化 (AS) 是一种慢性炎症性疾病,其特点是动脉中积聚斑块.
- 了解AS进展和斑块稳定性背后的分子机制对于开发有效的治疗方法至关重要.
- 乳酸 (LTF) 已显示出潜在的抗炎和抗氧化特性,但其在AS中的作用仍未完全阐明.
研究的目的:
- 调查乳酸铁素 (LTF) 在动脉样硬化 (AS) 中的作用.
- 探索LTF在AS中的作用的潜在机制,特别是与自的关系.
- 评估LTF作为AS进展和斑块稳定性的潜在预测生物标志物.
主要方法:
- 从对照组,冠状动脉疾病 (CHD) 和突然冠状动脉死亡 (SCD) 组对人类冠状动脉组织的分析.
- 在人体组织中评估LTF,P62和4-hydroxynonenal (4-HNE) 表达.
- 建立和分析具有自抑制的ApoE-/- AS小鼠模型.
- 在体外研究中,使用牛-LDL诱导的THP-1泡细胞模型来研究LTF和基因沉默后与自相关的蛋白质表达.
主要成果:
- 在SCD组中,斑块稳定性明显较低,LTF,P62和4-HNE水平增加与稳定性下降和AS进展相关.
- 在AS小鼠中,自抑制恶化了狭窄,增加了死核和泡细胞沉积,并减少了LTF表达.
- 在体外,THP-1细胞中的LTF沉默损害了自,促进了4-HNE的积累,并改变了Bcl-2/Bax比率,表明亡增加.
结论:
- 乳酸 (LTF) 表达与AS进展和减少斑块稳定性有关.
- 通过调节自和激活AMPK/mTOR通路,LTF可能会对AS产生保护作用.
- 作为动脉样硬化的潜在预测生物标志物,LTF具有前景.
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