粘着斑激酶驱动Rho/ROCK和mTOR信号传导以保护和增强主动脉夹层。

Suppr 超能文献

核心技术专利：CN118964589B侵权必究

Suppr 超能文献

核心技术专利：CN118964589B侵权必究

Zhou Zhen, Guan Pujun, Sarkar Ripon, Yu Yang, Richard Alexis, Weiss Dar, Kawamura Yuki, Zhang Chen, Li Yanming, Vaisar Tomas, Martin Daniel R, Buja L Maximillian, Li Zhouxuan, Venkatachalam Kartik, Shen Ying H, LeMaire Scott A, Humphrey Jay D, Milewicz Dianna M

Division of Medical Genetics, Department of Internal Medicine, The University of Texas Health Science Center at Houston McGovern Medical School, Houston, Texas, USA.

Division of Medical Genetics, Department of Internal Medicine, The University of Texas Health Science Center at Houston McGovern Medical School, Houston, Texas, USA; Department of Cardiac Surgery, The First Hospital of China Medical University, Shenyang, China.

JACC Basic Transl Sci. 2025 Aug 2;10(9):101353. doi: 10.1016/j.jacbts.2025.101353.

Dysfunctional mechanosensing via focal adhesions (FAs) significantly contributes to thoracic aortic dissection in the β-aminopropionitrile mouse model by triggering FA kinase activation and subsequent Rho/ROCK and mTOR signaling pathways. The present findings indicate that these signaling pathways play distinct roles in ascending vs descending dissections. Specifically, in the ascending aorta, smooth muscle cell FA kinase-Rho/ROCK signaling acts as a beneficial adaptive mechanism to prevent dissections, whereas mTOR signaling is pathogenic and contributes to dissections.

在β-氨基丙腈小鼠模型中，通过粘着斑（FAs）的机械传感功能失调会触发粘着斑激酶激活以及随后的Rho/ROCK和mTOR信号通路，从而显著导致胸主动脉夹层形成。目前的研究结果表明，这些信号通路在升主动脉夹层与降主动脉夹层中发挥着不同作用。具体而言，在升主动脉中，平滑肌细胞粘着斑激酶-Rho/ROCK信号作为一种有益的适应性机制来预防夹层形成，而mTOR信号则具有致病性并促使夹层形成。