The coordinated generation of mechanical forces by cardiac myocytes is required for proper heart function. Myofibrils are the functional contractile units of force production within individual cardiac myocytes. At the molecular level, myosin motors form cross‐bridges with actin filaments and use ATP to convert chemical energy into mechanical forces. The energetic efficiency of the cross‐bridge cycle is influenced by the viscous damping of myofibril contraction. The viscoelastic response of myofibrils is an emergent property of their individual mechanical components. Previous studies have implicated titin‐actin interactions, cell‐ECM adhesion, and microtubules as regulators of the viscoelastic response of myofibrils. Here we probed the viscoelastic response of myofibrils using laser‐assisted dissection. As a proof‐of‐concept, we found actomyosin contractility was required to endow myofibrils with their viscoelastic response, with blebbistatin treatment resulting in decreased myofibril tension and viscous damping. Focal adhesion kinase (FAK) is a key regulator of cell‐ECM adhesion, microtubule stability, and myofibril assembly. We found inhibition of FAK signaling altered the viscoelastic properties of myofibrils. Specifically, inhibition of FAK resulted in increased viscous damping of myofibril retraction following laser ablation. This damping was not associated with acute changes in the electrophysiological properties of cardiac myocytes. These results implicate FAK as a regulator of mechanical properties of myofibrils.

中文翻译：

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粘着斑激酶的抑制增加心肌细胞中的肌原纤维粘度。

心肌细胞协调产生机械力是正常心脏功能所必需的。肌原纤维是单个心肌细胞内产生力的功能性收缩单位。在分子水平上，肌球蛋白马达与肌动蛋白丝形成交叉桥，并利用 ATP 将化学能转化为机械力。跨桥循环的能量效率受肌原纤维收缩的粘性阻尼的影响。肌原纤维的粘弹性反应是其各个机械组件的一种新兴特性。以前的研究表明肌动蛋白-肌动蛋白相互作用、细胞-ECM 粘附和微管是肌原纤维粘弹性反应的调节剂。在这里，我们使用激光辅助解剖探测了肌原纤维的粘弹性反应。作为概念验证，我们发现肌动球蛋白收缩是赋予肌原纤维粘弹性反应所必需的，blebbistatin 治疗导致肌原纤维张力和粘性阻尼降低。粘着斑激酶 (FAK) 是细胞-ECM 粘附、微管稳定性和肌原纤维组装的关键调节剂。我们发现抑制 FAK 信号改变了肌原纤维的粘弹性。具体而言，FAK 的抑制导致激光消融后肌原纤维回缩的粘性阻尼增加。这种阻尼与心肌细胞电生理特性的急性变化无关。这些结果暗示 FAK 作为肌原纤维机械性能的调节剂。blebbistatin 治疗导致肌原纤维张力和粘性阻尼降低。粘着斑激酶 (FAK) 是细胞-ECM 粘附、微管稳定性和肌原纤维组装的关键调节剂。我们发现抑制 FAK 信号改变了肌原纤维的粘弹性。具体而言，FAK 的抑制导致激光消融后肌原纤维回缩的粘性阻尼增加。这种阻尼与心肌细胞电生理特性的急性变化无关。这些结果暗示 FAK 作为肌原纤维机械性能的调节剂。blebbistatin 治疗导致肌原纤维张力和粘性阻尼降低。粘着斑激酶 (FAK) 是细胞-ECM 粘附、微管稳定性和肌原纤维组装的关键调节剂。我们发现抑制 FAK 信号改变了肌原纤维的粘弹性。具体而言，FAK 的抑制导致激光消融后肌原纤维回缩的粘性阻尼增加。这种阻尼与心肌细胞电生理特性的急性变化无关。这些结果暗示 FAK 作为肌原纤维机械性能的调节剂。FAK 的抑制导致激光消融后肌原纤维回缩的粘性阻尼增加。这种阻尼与心肌细胞电生理特性的急性变化无关。这些结果暗示 FAK 作为肌原纤维机械性能的调节剂。FAK 的抑制导致激光消融后肌原纤维回缩的粘性阻尼增加。这种阻尼与心肌细胞电生理特性的急性变化无关。这些结果暗示 FAK 作为肌原纤维机械性能的调节剂。