由循环的活性氧物种激活的Hippo通路在急性损伤后调解心脏扩张性功能障碍
Xiao Han1, Quan Hong1, Fei Peng1
1Department of Nephrology, First Medical Center of Chinese People's Liberation Army (PLA) General Hospital, Chinese PLA Institute of Nephrology, National Key Laboratory of Kidney Diseases, National Clinical Research Center for Chronic Kidney Diseases, Beijing Key Laboratory of Kidney Diseases Research, Beijing 100853, China.
Biochimica et biophysica acta. Molecular basis of disease
|April 22, 2024
概括
在急性损伤后,循环的活性氧物种 (ROS) 介导心脏功能障碍. ROS激活Mst1/Hippo通路,导致心脏问题,并为心脏脏综合征提供新的治疗点.
科学领域:
- 心脏病学 心脏病学
- 腎臟病學 (nephrology) 是一種醫學.
- 生物化学 生物化学
背景情况:
- 急性损伤 (AKI) 可以导致心脏功能障碍,但机制尚不清楚.
- 氧化应激与AKI后的心脏与脏相互作用有关.
研究的目的:
- 调查循环活性氧物种 (ROS) 在缺血-再输损伤 (IRI) 后调解心脏功能障碍中的作用.
- 探索Mst1/Hippo通路在这个过程中的参与.
主要方法:
- 在小鼠中诱导脏IRI.
- 评估心脏功能,氧化应激,ATP水平和分支链氨基酸 (BCAA) 积累.
- 使用天治疗 (ROS清除剂).
- 在体外研究中,使用暴露于过氧化 (H2O2) 的Mst1-倒置和Mst1-过度表达心肌细胞.
主要成果:
- 脏IRI诱导了透支功能障碍,心脏ATP减少,氧化应激增加和BCAA积累.
- 循环中的ROS水平在脏,循环和心脏连续增加.
- 坦波尔治疗改善了心脏功能,并缓解了Mst1/Hippo通路的激活.
- 心肌细胞中Mst1/Hippo通路的激活与氧化应激和BCAA代谢不良有关.
结论:
- 在脏IRI之后循环的ROS激活了心肌中的Mst1/Hippo通路.
- 这种激活会导致心脏的氧化应激和腹功能障碍.
- 这些发现表明,针对ROS和Mst1/Hippo通路,针对心综合征的潜在治疗策略.
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