在内动脉瘤中,METTL3通过m6A-AMPK轴促进血管稳定
Zhentao Guo1, Yuan Zhong1, Zhixu Ming1
1Department of Neurosurgery, Qilu Hospital (Qingdao) of Shandong University, 758 Hefei Road, Qingdao, 266000, Shandong, China.
Scientific reports
|November 25, 2025
概括
低调METTL3与内动脉瘤 (IAs) 有关. METTL3通过AMPK调节血管光滑肌肉细胞表型,抑制增殖和迁移,从而防止IA的发展.
科学领域:
- 心血管生物学 心血管生物学
- 分子生物学分子生物学
- 遗传学 遗传学 是一个
背景情况:
- 内动脉瘤 (IA) 是一种严重的脑血管疾病.
- 一种mRNA甲基转移酶METTL3与心血管疾病有关,但其在IA中的作用尚不清楚.
研究的目的:
- 研究METTL3在内动脉瘤 (IA) 发育中的作用.
- 探索涉及AMPK信号通路的潜在分子机制.
主要方法:
- 分析了IA患者的METTL3表达和老鼠IA模型.
- 使用细胞培养 (VSMC) 和使用METTL3操纵的体内模型.
- 评估基因表达,细胞增殖,迁移,亡和巨细胞透.
主要成果:
- 在IA患者中,METTL3的下调和与AMPK表达相关.
- 在VSMC中METTL3过度表达上调收缩标志物和下调炎症基因,AMPK抑制可以逆转效应.
- 过度表达METTL3改善了大鼠IA模型血管形态,并减少了巨细胞的透.
结论:
- METTL3通过AMPK通路调节血管光滑肌肉细胞的表型转变.
- METTL3抑制VSMC的增殖/迁移,促进亡,并抑制巨细胞的透,从而阻碍IA的进展.
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