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在ANK缺陷中介的细胞酸积累促进了大动脉动脉瘤

Hao Wu¹, Zhiqing Li¹, Liu Yang^1,2

¹Department of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling (H.W., Z.L., L.Y., S.Y., Yanjie Li, W.L., Yiran Li, Z.G., Y.S., X.Y., J.H., F.Y., Y.F., W.K.), School of Basic Medical Sciences, Peking University, Beijing, China.

Circulation research

|November 8, 2024

概括

血管光滑肌细胞ANK缺乏增加酸盐,通过激活炎症基因促进大动脉动脉瘤 (AA). 向酸盐运输为AA处理提供了一个新的策略.

科学领域:

生物化学生物化学
血管生物学血管生物学
代谢学代谢学代谢学

背景情况:

酸盐的代谢和运输与各种疾病有关.
血管酸盐调节在大动脉动脉瘤 (AA) 发展中的作用尚不清楚.

研究的目的:

调查酸盐及其载体ANK在AA发展中的作用.
阐明连接ANK缺乏,酸盐积累和AA病变的分子机制.

主要方法:

未定位的代谢组在AA组织中确定了高调的三酸循环代谢产物.
在Ang II和CaPO4诱导的AA模型中使用了血管光滑肌细胞 (VSMC) 特定的Ank淘汰赛小鼠.

主要成果:

在人类和小鼠AA组织中观察到酸盐的增加和ANK的减少.
在VSMC中ANK缺乏促进了AA的形成,而ANK过度表达则抑制了它.
ANK 缺乏导致细胞质酸盐积累,增强了基因素乙化,并激活了VSMCs中的炎症基因转录.

结论:

由ANK缺陷驱动的酸盐积累通过一种促炎性VSMC表型促进AA病原体.
针对ANK介导的酸盐运输,为AA提供了潜在的诊断和治疗策略.

关键词:

化症是一种无化症.一个大动脉动脉瘤.酸是一种酸.基因组基因组基因组肌肉,光滑的,血管的肌肉.

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