Cardiac fibroblasts are interspersed within mammalian cardiac tissue. Fibroblasts are mechanically passive; however, they may communicate electrically with cardiomyocytes via gap junctions and thus affect the electrical and mechanical activity of myocytes.

Several in-silico studies at both cellular (0D) and ventricular (3D) levels analysed the effects of fibroblasts on the myocardial electrical function. However, none of them addressed possible effects of fibroblast-myocyte electrical coupling to cardiomyocyte mechanical activity.

In this paper, we propose a mathematical model for studying both electrical and mechanical responses of the human cardiomyocyte to its electrotonic interaction with cardiac fibroblasts.

Our simulations have revealed that electrotonic interaction with fibroblasts affects not only the mechanical activity of the cardiomyocyte, comprising either moderate or significant reduction of contractility, but also the mechano-calcium and mechano-electric feedback loops, and all these effects are enhanced as the number of coupled fibroblasts is increased.

Obtained results suggest that moderate values of the myocyte-fibroblast gap junction conductance (less than 1 nS) can be attributed to physiological conditions, contrasting to the higher values (2 nS and higher) proper rather for pathological situations (e.g. for infarct and/or border zones), since all mechanical indexes falls down dramatically in the case of such high conductance.

心脏成纤维细胞散布在哺乳动物心脏组织内。成纤维细胞在机械上是被动的；然而，它们可能通过间隙连接与心肌细胞进行电交流，从而影响心肌细胞的电和机械活动。

细胞 (0D) 和心室 (3D) 水平的几项计算机模拟研究分析了成纤维细胞对心肌电功能的影响。然而，它们都没有解决成纤维细胞-心肌细胞电耦合对心肌细胞机械活动的可能影响。

在本文中，我们提出了一个数学模型，用于研究人类心肌细胞对其与心脏成纤维细胞的电子相互作用的电和机械反应。

我们的模拟表明，与成纤维细胞的电渗相互作用不仅影响心肌细胞的机械活动，包括收缩力的中度或显着降低，而且还会影响机械-钙和机械-电反馈回路，并且所有这些影响都随着数量的增加而增强。成纤维细胞的数量增加。

获得的结果表明，肌细胞 - 成纤维细胞间隙连接电导的中等值（小于 1 nS）可归因于生理条件，与更高的值（2 nS 和更高）相反，而不是病理情况（例如，对于梗塞和/或边界区域），因为在如此高电导的情况下，所有机械指标都会急剧下降。