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PIASy缺乏会通过TGF-β/Smad2/3通路缓解胸前大动脉动脉瘤的形成

Dafu Shen^1,2, Hui Zheng³, Kejie Shao⁴

¹Department of Cardiovascular Surgery, the First Affiliated Hospital of Soochow University, Suzhou, China.

Journal of thoracic disease

|June 18, 2025

概括

激活STAT 4 (PIASy) 上调的蛋白抑制剂通过改变血管光滑肌细胞 (VSMC) 现型来促进胸前大动脉动脉瘤 (TAA). 抑制PIASy通过通过TGF-β/Smad通路维持VSMC分化来保护TAA.

科学领域:

心血管生物学心血管生物学
疾病的分子机制.
血管光滑肌肉细胞生物学

背景情况:

胸前动脉动脉瘤 (TAA) 是一种危及生命的心血管疾病,其分子基础尚未完全理解.
血管光滑肌细胞 (VSMC) 的表型调制是TAA病变发生的关键因素.
在TAA进展过程中,激活STAT 4 (PIASy) 的蛋白抑制剂在VSMC中的作用在很大程度上尚未被探索.

研究的目的:

在TAA的背景下调查PIASy的功能.
阐明PIASy对VSMC行为和TAA中相关信号通路的调节效应.

主要方法:

在人类和小鼠TAA组织中量化PIASy表达,使用RT-qPCR和Western blot.
通过血管激素II输液建立TAA的*in vivo*小鼠模型.
在MOVAS细胞中使用PIASy倒置和转录组分析 (RNA测序) *in vitro*评估PIASy的作用.

主要成果:

在人类和小鼠TAA组织中,PIASy表达显著上调.
在VSMC中,PIASy的抑制阻止了从收缩型转变为分泌型的表型,从而保留了收缩性标记物.
PIASy通过TGF-β/Smad2/3信号通路调节VSMC分化,PIASy缺陷可以逆转AngII诱导的抑制.

结论:

失去PIASy通过TGF-β/Smad通路调节VSMC分化,从而保护TAA.
准PIASy为TAA预防和治疗提供了一个潜在的治疗策略.

关键词:

胸前大动脉动脉瘤 (TAA) 发生现象型迅速迅速的激活STAT4 (PIASy) 的蛋白质抑制剂转化生长因子-β (TGF-β) 的转化生长因子血管光滑肌细胞 (VSMC) 是一种

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