Kamkin Andre, Kiseleva Irina, Lozinsky Ilya, Wagner Kay-Dietrich, Isenberg Gerrit, Scholz Holger
Department of Fundamental and Applied Physiology, State Medical University of Russia, Ostrovitjanova Str. 1, 117997 Moscow, Russia
Institute of Physiology, Humboldt-University, Charité, Tucholskystrasse 2, 10117 Berlin, Germany
Cardiac fibroblasts can respond to mechanical deformation of the plasma membrane with characteristic changes of their membrane potential. These changes of fibroblasts membrane potential are determined by operation of stretch-inactivated channels. These channels, mainly permeable for sodium ions, are activated by compression of the cell leading to depolarization, and are inactivated by stretch, which in turn leads to hyperpolarization. Thus, cardiac fibroblasts function as mechanoelectric transducers in the heart and represent the cellular substrate for a cardiac mechanoelectrical feedback mechanism. Increased sensitivity of the cardiac fibroblasts to mechanical changes contributes to electrical instability and arrhythmia after myocardial infarction. Recent findings indicate that these processes involve the transfer of electrical signals via gap junctions. In this article we will discuss the recent progress in the electrophysiology of cardiac fibroblasts and their role in mechanoelectric feedback in healthy and diseased hearts.
心脏成纤维细胞可通过其膜电位的特征性变化对质膜的机械变形作出反应。成纤维细胞膜电位的这些变化由拉伸失活通道的运作所决定。这些通道主要对钠离子通透,通过细胞受压而激活,导致去极化,通过拉伸而失活,进而导致超极化。因此,心脏成纤维细胞在心脏中起着机电换能器的作用,代表了心脏机电反馈机制的细胞基础。心脏成纤维细胞对机械变化敏感性的增加会导致心肌梗死后的电不稳定和心律失常。最近的研究结果表明,这些过程涉及通过缝隙连接传递电信号。在本文中,我们将讨论心脏成纤维细胞电生理学的最新进展及其在健康和患病心脏的机电反馈中的作用。