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损坏的CAMK4活动限制了动脉样硬化和重编程骨髓形成

Azuah L Gonzalez¹, Cristina M Youwakim^2,3, Brenda F Leake^2,3

¹Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN. (A.L.G., M.M.D., A.B.C., K.C.V., A.C.D.).

Arteriosclerosis, thrombosis, and vascular biology

|May 8, 2025

概括

向/卡尔莫杜林依赖蛋白激酶IV (CaMK4) 可能会减少动脉样硬化的进展. 在小鼠中,CaMK4的丧失导致了较小,更稳定的病变和亲修复性髓状细胞表型,这表明了新的治疗标.

科学领域:

心血管生物学心血管生物学
免疫学免疫学免疫学
分子医学是分子医学.

背景情况:

慢性炎症显著推动动脉样硬化心血管疾病.
在人类动脉硬性斑块中观察到/卡尔莫杜林依赖蛋白激酶IV (CaMK4) 的表达增加.
在斑块巨细胞中CaMK4的含量升高,这表明它在动脉样硬化中起着作用.

研究的目的:

调查CaMK4在促进炎症和降低动脉样硬化症解决的作用.
为了确定CaMK4是否调节对高胆固醇血症的骨髓构成反应.

主要方法:

产生的淘汰赛小鼠缺乏功能性的CaMK4 (Camk4-/-).
使用AAV8-PCSK9和高脂肪/高胆固醇饮食诱导的高胆固醇血症.
分析了病变的大小,稳定性,单细胞群和骨髓原生细胞水平.

主要成果:

卡姆克4-/-小鼠表现出较小,更稳定的动脉样硬化病变.
对CaMK4的损失导致了外周单细胞化,而单细胞的炎症性较小.
卡姆克4-/-单细胞显示了基因表达的改变 (ATF6,Nr4a1) 和受损的贩运,巨细胞显示了亲修复的表型.

结论:

在高胆固醇血症期间,CaMK4通过ATF6-介导的转录来调节骨髓形成.
对CaMK4的损失促进了髓状细胞中的亲修复性表型.
向CaMK4是一个潜在的动脉样硬化治疗策略.

关键词:

动脉样硬化动脉样硬化骨髓骨髓骨髓骨髓骨髓巨细胞是什么?巨细胞是什么?单细胞 (Monocytes) 是一种单细胞.骨髓形成 (myelopoiesis) 是一种形成骨髓的过程.

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