血管紧张素II在心房结构重塑中的作用：血管紧张素II/ Janus激酶/信号转导和转录激活因子3信号通路的作用
Angiotensin II in atrial structural remodeling: the role of Ang II/JAK/STAT3 signaling pathway.
作者信息
Zheng Liuying, Jia Xiaogang, Zhang Cheng, Wang Dong, Cao Zhongnan, Wang Jin, Du Xinping
机构信息
The Fifth Central Hospital of Tianjin Tianjin, China.
Peking University First Hospital Beijing, China.
出版信息
Am J Transl Res. 2015 Jun 15;7(6):1021-31. eCollection 2015.
Ang II/JAK/STAT3 signaling pathway is known to be involved in atrial remodeling associated with development and progression of atrial fibrillation. In the present study, we used in vivo animal model and human atrial specimens to further characterize the role of this pathway in the atrial structural remodeling. We observed an elevated level of Ang II in the atrial samples of AF patients. This increase in Ang II was accompanied by increased expression of collagens I and III, MMP1, MMP2 and elevated phosphorylation of STAT3. Using rat models, we demonstrated that Ang II infusion induced profound changes in the level of apoptosis, expression of collagen subtypes I and III, caspase-3, caspase-8, MMP1, MMP2 and redistribution of cytochrome C. The data further support the key role of Ang II in the development of AF and highlight the specific mechanisms and changes associated with this process.
已知血管紧张素II/Janus激酶/信号转导和转录激活因子3（Ang II/JAK/STAT3）信号通路参与了与心房颤动发生和发展相关的心房重构。在本研究中，我们使用体内动物模型和人类心房标本，进一步明确该通路在心房结构重构中的作用。我们观察到房颤患者心房样本中血管紧张素II水平升高。血管紧张素II的这种增加伴随着I型和III型胶原蛋白、基质金属蛋白酶1（MMP1）、基质金属蛋白酶2（MMP2）表达的增加以及信号转导和转录激活因子3的磷酸化水平升高。使用大鼠模型，我们证明血管紧张素II输注可诱导细胞凋亡水平、I型和III型胶原蛋白亚型、半胱天冬酶-3、半胱天冬酶-8、基质金属蛋白酶1、基质金属蛋白酶2的表达以及细胞色素C的重新分布发生显著变化。这些数据进一步支持了血管紧张素II在房颤发生中的关键作用，并突出了与此过程相关的具体机制和变化。
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