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在动脉样硬化中,NAD代谢调节巨细胞的增殖

Satyesh K Sinha^1,2,3, Chantle R Swichkow^1,2,3, Lia Farahi^1,2,3

¹Department of Medicine/Division of Cardiology (S.K.S., C.R.S., L.F., M.P., C.P., Z.Z., J.J.M., R.C.D., D.M.S., A.J.L.), University of California Los Angeles.

Arteriosclerosis, thrombosis, and vascular biology

|September 11, 2025

概括

尼古丁胺 N-甲基转移酶 (NNMT) 通过改变巨细胞中的尼古丁胺腺素二核酸 (NAD) 水平来驱动动动脉硬化. 抑制NNMT或促进NAD代谢可以减少病变的发生,并改善巨细胞的功能.

科学领域:

心血管研究研究心血管研究
代谢性疾病代谢性疾病
分子遗传学分子遗传学

背景情况:

之前已经确定了与动脉样硬化相关的染色体9位点.
现在已经确定NNMT (尼古丁胺胺N-甲基转移酶) 是病因基因.
这种机制涉及尼古丁胺的恢复到尼古丁胺胺二核酸 (NAD).

研究的目的:

研究NAD水平在巨细胞增殖和动脉样硬化中的亡中的作用.
为了确定NNMT抑制是否影响动脉样硬化进展.

主要方法:

在巨细胞的功能研究中获得/损失.
全球NNMT抑制使用反感性寡核酸.
使用siRNA在肝脏和脂肪中选择性NNMT抑制.
从NNmt淘汰赛小鼠移植骨髓.
对巨细胞CD38表达的分析.
来自异构卵性NNmt淘汰赛小鼠的巨细胞培养.

主要成果:

全球NNMT抑制显著减少了小鼠的动脉样硬化病变区域.
选择性NNMT抑制在肝脏/脂肪细胞的效果是最小的.
来自Nnmt淘汰赛小鼠的骨髓减少了病变巨细胞的增殖和增加了亡.
减少CD38表达减少了巨细胞的增殖和动脉样硬化.
来自Nnmt淘汰赛小鼠的巨体显示出减少的增殖,增加的亡,以及更高的NAD/NADH比率.

结论:

尼古丁胺的挽救和NAD的周转对于巨细胞的增殖和动脉样硬化中的生存至关重要.
在巨细胞中,NNMT在调节NAD代谢方面发挥着关键作用.
准NNMT或NAD代谢是一种潜在的动脉样硬化治疗策略.

关键词:

灭症 (apoptosis) 是一种死亡的过程.动脉样硬化动脉样硬化细胞的增殖细胞的增殖.巨细胞是一个巨细胞.尼古丁胺胺 N-甲基转移酶

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