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细胞衰老有助于大弹性动脉硬化和内皮功能障碍随着衰老:通过老化治疗改善

Zachary S Clayton¹, Matthew J Rossman¹, Sophia A Mahoney¹

¹Department of Integrative Physiology, University of Colorado Boulder (Z.S.C., M.J.R., S.A.M., R.V., G.S.M., D.A.H., N.S.V., N.T.G., A.G.L., K.R.L., V.E.B., D.R.S.).

Hypertension (Dallas, Tex. : 1979)

|August 18, 2023

概括

细胞衰老驱动与年龄有关的大动脉硬化和内皮功能障碍. 用老化剂清除衰老细胞通过减少大动脉硬性和增强内皮功能来改善血管功能.

科学领域:

老年学是一门学科.
血管生物学血管生物学
细胞生物学细胞生物学

背景情况:

与年龄相关的血管功能障碍,包括大动脉硬化和内皮功能障碍,是严重的健康问题.
细胞衰老和与衰老相关的分泌表型 (SASP) 与衰老过程有关.
老化和SASP在与年龄有关的大动脉变化中的具体作用需要进一步阐明.

研究的目的:

研究细胞衰老和SASP对与年龄有关的大动脉硬化和内皮功能障碍的贡献.
评估老化干预措施在缓解这些与年龄相关的血管变化的治疗潜力.

主要方法:

使用p16-3MR小鼠进行使用甘西克洛维尔 (GCV) 的衰老细胞的遗传清除.
用老化药物ABT-263.3治疗老年C57BL/6N小鼠.
通过脉冲波速度 (PWV) 和ex vivo弹性模量评估大动脉刚性.
通过 carotid 动脉内皮依赖扩张 (EDD) 评估内皮功能.
分析了血SASP因子及其与血管功能的关联.

主要成果:

在老老鼠中,GCV治疗显著降低了大动脉硬性 (PWV),达到与年轻小鼠相似的水平.
在老年小鼠中,ABT-263还降低了主动脉硬度和偶然原.
来自衰老细胞的血诱导了大动脉硬化,这种效应被GCV消除了.
衰老细胞清除通过增加氧化 (NO) 的生物可用性和减少氧化应激,改善了内皮功能 (EDD).
与NO信号相关的特定SASP因素与改进的NO介导EDD相关.

结论:

细胞衰老和SASP是血管衰老的关键因素,特别是大动脉硬化和内皮功能障碍.
老化疗法在改善与年龄相关的血管衰退和改善心血管健康方面显示出显著的前景.

关键词:

衰老的衰老衰老的衰老大动脉硬性大动脉硬细胞衰老细胞衰老脑内皮的内皮功能.与衰老相关的分泌表现型

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