TWIK-related K⁺ channel (TREK-1) two-pore-domain potassium (K_2P) channels mediate background potassium currents and regulate cellular excitability in many different types of cells. Their functional activity is controlled by a broad variety of different physiological stimuli, such as temperature, extracellular or intracellular pH, lipids and mechanical stress.

By linking cellular excitability to mechanical stress, TREK-1 currents might be important to mediate parts of the mechanoelectrical feedback described in the heart. Furthermore, TREK-1 currents might contribute to the dysregulation of excitability in the heart in pathophysiological situations, such as those caused by abnormal stretch or ischaemia-associated cell swelling, thereby contributing to arrhythmogenesis.

In this review, we focus on the functional role of TREK-1 in the heart and its putative contribution to cardiac mechanoelectrical coupling. Its cardiac expression among different species is discussed, alongside with functional evidence for TREK-1 currents in cardiomyocytes. In addition, evidence for the involvement of TREK-1 currents in different cardiac arrhythmias, such as atrial fibrillation or ventricular tachycardia, is summarized. Furthermore, the role of TREK-1 and its interaction partners in the regulation of the cardiac heart rate is reviewed. Finally, we focus on the significance of TREK-1 in the development of cardiac hypertrophy, cardiac fibrosis and heart failure.

TWIK 相关 K ⁺通道 (TREK-1) 双孔域钾 (K _2P ) 通道介导背景​​钾电流并调节许多不同类型细胞的细胞兴奋性。它们的功能活动受多种不同生理刺激的控制，例如温度、细胞外或细胞内 pH 值、脂质和机械应力。

通过将细胞兴奋性与机械应力联系起来，TREK-1 电流可能对调节心脏中描述的部分机械电反馈很重要。此外，TREK-1 电流可能会导致病理生理情况下心脏兴奋性失调，例如由异常拉伸或缺血相关细胞肿胀引起的兴奋性失调，从而导致心律失常。

在这篇综述中，我们关注 TREK-1 在心脏中的功能作用及其对心脏机电耦合的假定贡献。讨论了它在不同物种中的心脏表达，以及心肌细胞中 TREK-1 电流的功能证据。此外，总结了 TREK-1 电流参与不同心律失常（如房颤或室性心动过速）的证据。此外，还审查了 TREK-1 及其相互作用伙伴在调节心率中的作用。最后，我们关注 TREK-1 在心脏肥大、心脏纤维化和心力衰竭发展中的重要性。