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细胞质和核NFATc3协同促进血管光滑肌肉细胞功能障碍,并驱动大动脉动脉瘤和剖析

Xiu Liu¹, Li Zhao¹, Deshen Liu¹

¹Department of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.

Acta pharmaceutica Sinica. B

|July 23, 2025

概括

血管光滑肌细胞 (VSMCs) 中激活T细胞c3 (NFATc3) 的核因子通过降解细胞外基质驱动大动脉动脉瘤和剖析 (AAD). 抑制NFATc3可能为AAD提供一种新的治疗策略.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
血管细胞生物学血管细胞生物学

背景情况:

大动脉动脉瘤和剖析 (AAD) 涉及血管光滑肌细胞 (VSMC) 功能障碍和细胞外基质 (ECM) 退化.
活化T细胞c3 (NFATc3) 的核因子在VSMCs在AAD发病过程中的作用尚不清楚.

研究的目的:

调查在AAD进展过程中VSMCs中NFATc3的功能.
阐明NFATc3影响AAD发育的分子机制.

主要方法:

在人类和小鼠AAD组织中分析NFATc3水平.
生成VSMC特定的NFATc3淘汰和过度表达的小鼠模型.
评估ECM降解,VSMC表型和分子信号通路.
在体内使用卡巴米奎因向真核延长因子2 (eEF2) 的研究.

主要成果:

在人类和小鼠AAD中观察到细胞质和核NFATc3水平升高.
删除VSMC-NFATc3减轻了AAD进展,减少了ECM降解,并保留了VSMC收缩表型.
核NFATc3对MMP9和MMP2进行了上调,促进了ECM的降解.
NFATc3抑制了eEF2酸化,导致VSMC的表型切换.
在VSMC-NFATc3过度表达的小鼠中,卡巴米治疗抑制了AAD的发展.

结论:

VSMC-NFATc3促进了VSMC的表型切换和ECM降解,加剧了AAD.
NFATc3代表了AAD预防和治疗的潜在治疗标.

关键词:

大动脉动脉瘤和剖析细胞外基质降解的细胞外基质降解这就是MMP2的MMP2.在MMP9中,MMP9是MMP9.在 NFATc3 中.翻译延伸的延伸.eEF2EF2 是一个简单的.

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