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CTRP13通过AMPK/KLF4途径缓解内皮细胞铁:对动脉样硬化保护的影响

Jie Du^1,2,3, Jianjun Wu^1,2, Youqi Zhang^1,2

¹Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China (mainland).

Medical science monitor : international medical journal of experimental and clinical research

|January 26, 2024

概括

C1q/瘤亡因子相关蛋白13 (CTRP13) 通过减少氧化应激和改善线粒体功能来保护人类脉内皮细胞免受铁亡. CTRP13激活AMPK/KLF4通路,为内皮功能障碍提供了一个新的治疗点.

科学领域:

心血管生物学心血管生物学
细胞生物学细胞生物学
生物化学生物化学

背景情况:

已知C1q/瘤缩因子相关蛋白13 (CTRP13) 能维持内皮功能并表现出抗氧化特性.
CTRP13对人类静脉内皮细胞 (HUVECs) 铁亡的特定影响尚未完全阐明.
氧化低密度脂蛋白 (ox-LDL) 是已知的内皮细胞铁灭的诱导物.

研究的目的:

调查CTRP13在HUVEC中对ox-LDL诱导的铁亡的保护作用.
探索涉及AMPK/KLF4信号通路的潜在分子机制.

主要方法:

细胞活力通过细胞计数工具-8试验进行了评估.
用Mito-Tracker,JC-1和malondialdehyde测定来评估线粒体功能,活性氧物种 (ROS) 水平和脂质过氧化.
基因和蛋白质表达的铁亡标记物 (SLC7A11,GPX4) 和AMPK/KLF4通路通过RT-PCR,西斑和免疫光分析.

主要成果:

CTRP13治疗显著抑制了HUVECs中的ox-LDL诱导的铁亡,减少了ROS过量产生和改善了线粒体功能障碍.
CTRP13提高了抗氧化酶 (HO-1,SOD1,SOD2) 的调节,增加了p-AMPK/AMPK的表达,同时降低了KLF4的表达.
这些发现表明,CTRP13的保护作用是针对由铁死介导的内皮功能障碍.

结论:

CTRP13在HUVECs中显示出对ferroptosis的显著保护作用.
该机制涉及AMPK/KLF4通路的调节和抗氧化能力的增强.
CTRP13代表了一种潜在的治疗剂,可以预防内皮细胞铁和相关的血管疾病.

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