在缺血和再输血期间,JAK/STAT信号与心脏功能障碍有关
E Mascareno1, M El-Shafei, N Maulik
1Center for Cardiovascular and Muscle Research, Department of Anatomy and Cell Biology, State University of New York Health Science Center Brooklyn, Brooklyn, NY, USA.
Circulation
|July 18, 2001
概括
简氏激酶/信号传感器和转录激活器 (JAK/STAT) 途径的激活有助于心脏缺血. 抑制这种途径可以减少损伤,并在缺血/再输血后改善心脏功能.
科学领域:
- 心血管研究研究心血管研究
- 分子生物学分子生物学
- 病理生理学 病理生理学
背景情况:
- 心脏氨酸-动脉酶系统 (RAS) 的激活与缺血性损伤有关.
- ангиотензин II 信号激活细胞内通路,包括 JAK/STAT.
研究的目的:
- 研究JAK/STAT信号在心肌缺血/反损伤中的作用.
- 确定JAK/STAT激活是否有助于心脏损伤.
主要方法:
- 研究的成年大鼠心肌发生缺血/再输血.
- 分析了STAT 5A和STAT 6组件的激活.
- 使用的AT(1) 阻断剂 (洛萨坦) 和JAK2抑制剂 (tyrphostin AG490).
主要成果:
- 在缺血/再输血后,STAT 5A和STAT 6被激活.
- 激活的STATs上调了血管激素原 (ANG) 基因和mRNA.
- 抑制剂阻断了STAT/ANG促进体结合,减少了心脏病发作的大小,细胞亡,并改善了血液动力学.
结论:
- JAK/STAT通路的激活是心肌缺血病原发生的一个关键因素.
- 干扰JAK/STAT激活可以促进心脏功能恢复.
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