与Ca ((2+) 相关的信号和蛋白质酸化异常在电风暴的新实验模型中发挥着核心作用
Yukiomi Tsuji1, Mayumi Hojo, Niels Voigt
1Department of Cardiovascular Research, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan. y-tsuji@hh.iij4u.or.jp
Circulation
|May 11, 2011
概括
植入式心脏转换器-除器患者的电风暴 (ES) 涉及与Ca2+相关的蛋白质变化. 这项研究揭示了Ca2+) /calmodulin-dependent蛋白激酶II激活和斯福兰班脱酸化有助于ES心律失常的促进和功能障碍.
科学领域:
- 心脏病学 心脏病学
- 分子生物学分子生物学
- 电力生理学 电力生理学
背景情况:
- 电风暴 (ES) 是植入式心脏转换器-除器患者的严重并发症.
- 在ES背后的分子机制仍然不太清楚.
- 这项研究引入了一种用于研究ES的新型实验模型.
研究的目的:
- 研究 (Ca2+) 处理蛋白质改变在ES发展中的作用.
- 阐明ES中恶性循环的分子基础.
主要方法:
- 使用了一种具有完整心房阻塞和可植入心脏转换器-除器植入的子模型.
- 在心室组织中分析了Ca2+处理蛋白的表达和酸化.
- 评估了卡尔莫杜林抗剂 (W-7) 对ES和心脏功能的影响.
主要成果:
- 在ES子中,Ca2+/卡尔莫杜林依赖蛋白激酶II (CaMKII) 过酸化和索兰班脱酸化增加.
- 与非ES子相比,ES子的收缩功能障碍显著增加.
- 卡尔莫杜林抗剂治疗减少了CaMKII过酸化,抑制了心律失常,并改善了心脏功能.
结论:
- ES与CaMKII的显著激活和胺的脱酸化有关.
- 这些分子变化有助于促进ES中的心律失常和机械功能障碍.
- 准CaMKII可能为管理ES提供治疗策略.
相关概念视频
Calmodulin-dependent Signaling
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A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates all these signals and determines the likelihood of firing an action potential.
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.
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