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首页> 外文期刊>Pfluegers Archiv: European Journal of Physiology >TREK-1 protects the heart against ischemia-reperfusion-induced injury and from adverse remodeling after myocardial infarction
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TREK-1 protects the heart against ischemia-reperfusion-induced injury and from adverse remodeling after myocardial infarction

机译：Trek-1保护心脏免受缺血再灌注诱导的损伤和心肌梗死后的不利重塑

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摘要

The TWIK-related K+ channel (TREK-1) is a two-pore-domain potassium channel that produces background leaky potassium currents. TREK-1 has a protective role against ischemia-induced neuronal damage. TREK-1 is also expressed in the heart, but its role in myocardial ischemia-reperfusion (IR)-induced injury has not been examined. In the current study, we used a TREK-1 knockout (KO) mouse model to show that TREK-1 has a critical role in the cardiac I/R-induced injury and during remodeling after myocardial infarction (MI). At baseline, TREK-1 KO mice had similar blood pressure and heart rate as the wild-type (WT) mice. However, the lack of TREK-1 was associated with increased susceptibility to ischemic injury and compromised functional recovery following ex vivo I/R-induced injury. TREK-1 deficiency increased infarct size following permanent coronary artery ligation, resulting in greater systolic dysfunction than the WT counterpart. Electrocardiographic (ECG) analysis revealed QT interval prolongation in TREK-1 KO mice, but normal heart rate (HR). Acutely isolated TREK-1 KO cardiomyocytes exhibited prolonged Ca2+ transient duration associated with action potential duration (APD) prolongation. Our data suggest that TREK-1 has a protective effect against I/R-induced injury and influences the post-MI remodeling processes by regulating membrane potential and maintaining intracellular Ca2+ homeostasis. These data suggest that TREK-1 activation could be an effective strategy to provide cardioprotection against ischemia-induced damage.
机译：TWIK相关的K +通道（TREK-1）是一种两孔域钾通道，产生背景漏钾电流。 Trek-1对缺血引起的神经元损伤具有保护作用。 Trek-1也在心脏中表达，但其在心肌缺血再灌注（IR）诱导的损伤中的作用尚未得到检查。在目前的研究中，我们使用了Trek-1敲除（KO）小鼠模型，以表明Trek-1在心脏I / R诱导的损伤和心肌梗死后重塑时具有关键作用（MI）。在基线时，Trek-1 KO小鼠具有与野生型（WT）小鼠相似的血压和心率。然而，缺乏Trek-1与对缺血性损伤的易感性增加有关，并且在离体I / R诱导的损伤后损害功能恢复。 TREK-1缺乏症在永久性冠状动脉连接后增加梗塞大小，导致比WT对应物更大的收缩功能障碍。心电图（ECG）分析显示TREK-1 KO小鼠中的QT间隔延长，但正常的心率（HR）。急性分离的Trek-1 KO心肌细胞显示出与动作电位持续时间（APD）延长相关的延长CA2 +瞬态持续时间。我们的数据表明，Trek-1对I / R诱导的损伤具有保护作用，通过调节膜电位和维持细胞内Ca2 +稳态来影响MIE后改造过程。这些数据表明，Trek-1激活可能是提供心脏保护免受缺血诱导的损伤的有效策略。

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