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Stability of Genetically Engineered Cardiac Pacemaker - Role of Intracellular Ca{sup}(2+) Handling

机译:基因工程心脏起搏器的稳定性 - 细胞内Ca {sup}(2+)处理的作用

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Down-regulation of Kir2.1 channel reduces the inward-rectifier potassium current (i{sub}(K1)), and transforms excitable ventricular myocytes to pacemaker cells. This provides a possible bio-technique to induce a biological pacemaker, as an alternative to an implantable electronic pacemaker. However there are two fundamental issues: (i) the stability of the pacemaker activity; (ii) the critical size of the biological pacemaker necessary for robust pacing and driving the surrounding ventricular muscle. In this study, we address the two issues by computer modelling.
机译:基于kir2.1的缩小调节降低了向内整流钾电流(I {sub}(K1)),并将激发的心室肌细胞转化为起搏器细胞。这提供了一种诱导生物起搏器的可能生物技术,作为可植入电子起搏器的替代方案。然而,有两个基本问题:(i)起搏器活动的稳定性; (ii)生物起搏器的临界大小是鲁棒起搏和驾驶周围的心室肌肉所必需的。在这项研究中,我们通过计算机建模解决了这两个问题。

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