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在平滑肌细胞中的普列尼林-1促进了在弹性腺体病的超肌化

Junichi Saito^1,2,3, Jui M Dave^1,2,3, Freddy Duarte Lau^1,2

¹Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University, New Haven, CT 06511, USA.

|January 16, 2024

概括

在光滑肌细胞中的普列尼林-1 (PSEN-1) 通过激活Notch信号来驱动上动脉狭窄 (SVAS). 在这些细胞中抑制PSEN-1为像SVAS这样的弹性质缺陷性动脉疾病提供了一个有希望的治疗策略.

科学领域:

心血管生物学心血管生物学
分子遗传学分子遗传学
血管病理生理学

背景情况:

顺肌细胞 (SMC) 积累是弹性质缺陷动脉疾病的关键,例如上膜大动脉狭窄症 (SVAS).
弹性素不足会激活大动脉SMC中的Notch信号,但马分泌酶子单元presenilin (PSEN) -1和PSEN-2的具体作用尚不清楚.

研究的目的:

调查PSEN-1和PSEN-2在弹性质动脉病变和SVAS病变发生过程中的作用.
确定针对SMC中的PSEN-1是否可以成为SVAS的治疗策略.

主要方法:

利用遗传方法,包括细胞特异性基因删除 (内皮细胞和SMC),在老鼠模型中研究PSEN-1和PSEN-2功能.
采用了PSEN-1的药理抑制来评估其对疾病模型中SMC积累的影响.
评估了大动脉疾病的严重程度,SMC的扩散和生存率.

主要成果:

特定于内皮细胞的Psen1删除并没有挽救弹性质动脉动脉病.
在SMC中删除Psen1或在SMC中删除Psen2减弱的Notch信号和SMC增殖,减轻大动脉疾病.
在无弹性质小鼠中,SMC特异性的Psen1删除显示出强大的救援效应和增加的生存率.
药理上抑制PSEN-1减少了在弹性肌动脉病模型中的SMC积累.

结论:

SMC局部化的PSEN-1,而不是内皮PSEN-1,在弹性腺体病变的发病过程中起着至关重要的作用.
在SMC中准PSEN-1为治疗SVAS和相关的弹性质缺陷动脉疾病提供了可行的治疗途径.

关键词:

生物科学生物科学自然科学自然科学生理学生理学生理学

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