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棕海豚缺乏症在膜内皮细胞中引起NF-κB信号,并加剧大动脉膜重塑

Yingchun Han^1,2, Jichao Zhang^1,2, Zhao Yang¹

¹Beijing Anzhen Hospital, Capital Medical University, Beijing, China.

JACC. Basic to translational science

|December 14, 2023

概括

缺乏Palmd的小鼠表现出性大动脉膜疾病的特征. 恢复Palmd表达可以防止这种情况,突出其治疗潜力.

科学领域:

心血管生物学心血管生物学
分子生物学分子生物学
病理学病理学病理学

背景情况:

气性大动脉病 (CAVD) 的特征是大动脉的加厚和化.
内皮功能障碍和膜间歇性细胞激活有助于CAVD的发病.
在大动脉健康和疾病中的Palmd (Palmd) 的作用尚不清楚.

研究的目的:

调查Palmd在形大动脉病的发展中的作用.
阐明Palmd影响膜内皮细胞和NF-κB信号传递的分子机制.
在CAVD的小鼠模型中评估Palmd的治疗潜力.

主要方法:

对表现出CAVD特征的Palmd缺乏的老年小鼠的分析.
评估膜内皮细胞对振荡式剪切应力的反应.
研究Palmd与TNFAIP3相互作用蛋白1和NF-κB通路组件的相互作用.
在CAVD的小鼠模型中,腺相关病毒介导的Palmd基因传递.

主要成果:

缺乏Palmd的小鼠表现出大动脉门速度的增加,叶片的加厚和细胞外基质沉积.
帕尔姆德静止的膜内皮细胞在振荡式剪切应力下显示出对内皮到介质细胞过渡的敏感性增加.
失去Palmd会损害TNFAIP3依赖的deubiquitinating活动,导致IKBKG的ubiquitination和NF-κB的激活增加.
使用腺相关病毒过度表达Palmd在CAVD小鼠中改善了大动脉膜重塑.

结论:

帕尔姆德在维持大动脉的完整性和预防CAVD方面发挥着保护作用.
帕尔姆德通过调节IKBKG的TNFAIP3依赖的二维基化来调节NF-κB信号传递.
帕尔姆德代表了治疗形大动脉膜疾病的潜在治疗标.

关键词:

在 NF-κBB 中.甲状腺膜疾病甲状腺膜疾病细胞内皮细胞的内皮细胞.内皮细胞到介质细胞的转变 (EndMT)棕海豚棕海豚是什么意思门改造门改造门改造门改造门改造

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