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Transverse Aortic Constriction in Mice
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含有gp91(phox) 的NADPH氧化酶在小鼠血管素II诱导的心脏缩中的关键作用.

Jennifer K Bendall1, Alison C Cave, Christophe Heymes

  • 1Department of Cardiology, Guy's, King's and St Thomas' School of Medicine, King's College London, London, UK.

Circulation
|January 24, 2002
PubMed
概括

一种特定的NADPH氧化酶酶对于血管酶II诱导的心脏缩至关重要. 这一发现突出了潜在的治疗目标心脏病,独立于血压的影响.

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科学领域:

  • 心血管生物学 心血管生物学
  • 分子医学是分子医学.
  • 生物化学 生物化学

背景情况:

  • 众所周知, ангиотензин II 会导致心脏和血管平滑肌肉缩.
  • 一种细胞类型的NADPH氧化酶与血管光滑肌肉缩有关.
  • NADPH氧化酶在心脏缩中的作用以前没有研究过.

研究的目的:

  • 为了研究NADPH氧化酶在血管酶II诱导的心脏缩中的作用.

主要方法:

  • 缺乏NADPH氧化酶 (gp91(phox-/-)) 的gp91(phox) 子单元的小鼠和野生类型的小鼠接受了血管新素II输液.
  • 用心脏/体重比,基因表达,肌细胞大小和原含量来评估心脏缩.
  • 测量了心肌NADPH氧化酶活性.

主要成果:

  • ангиотензин II 在野生类型小鼠中显著增加心脏缩标志物,但在gp91(phox-/-) 小鼠中没有.
  • 在这两组中,缩血压保持不变.
  • 只有在野生型小鼠中, ангиотензин II 增加了心肌NADPH氧化酶活性.

结论:

  • 含有gp91 (((phox) 的NADPH氧化酶对于血管素II诱导的心脏缩至关重要.
  • 这种机制独立于血压变化而运作.
  • 准这种NADPH氧化酶可能为心脏缩提供一种新的治疗策略.