Both diastolic filling and systolic pumping of the heart are dependent on the passive stiffness characteristics of various mechanical elements of myocardium. However, the specific contribution from each element, including the extracellular matrix, actin filaments, microtubules, desmin intermediate filaments, and sarcomeric titin springs, remains challenging to assess. Recently, a mouse model allowing for precise and acute cleavage of the titin springs was used to remove one mechanical element after the other from cardiac fibers and record the effect on passive stiffness. It became clear that the stiffness contribution from each element is context-dependent and varies depending on strain level and the force component considered (elastic or viscous); elements do not act in isolation but in a tensegral relationship. Titin is a substantial contributor under all conditions and dominates the elastic forces at both low and high strains. The contribution to viscous forces is more equally shared between microtubules, titin, and actin. However, the extracellular matrix substantially contributes to both force components at higher strain levels. Desmin filaments may bear low stiffness. These insights enhance our understanding of how different filament networks contribute to passive stiffness in the heart and offer new perspectives for targeting this stiffness in heart failure treatment.

中文翻译：

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肌联蛋白在细胞骨架对心肌被动僵硬的贡献中占据中心地位

心脏的舒张期充盈和收缩期泵血均取决于心肌各种机械元件的被动刚度特性。然而，每个元素的具体贡献，包括细胞外基质、肌动蛋白丝、微管、结蛋白中间丝和肌节肌联蛋白弹簧，仍然难以评估。最近，一种允许精确而急剧地裂解肌腱弹簧的小鼠模型被用来从心脏纤维中移除一个又一个的机械元件，并记录对被动刚度的影响。很明显，每个元素的刚度贡献取决于上下文，并且根据应变水平和所考虑的力分量（弹性或粘性）而变化；元素并不是孤立地起作用，而是以张拉关系的形式起作用。肌联蛋白在所有条件下都是重要的贡献者，并且在低应变和高应变下主导弹力。微管、肌联蛋白和肌动蛋白对粘性力的贡献更为平均。然而，细胞外基质在较高应变水平下对两个力分量都有显着贡献。结蛋白丝可能具有较低的刚度。这些见解增强了我们对不同细丝网络如何导致心脏被动僵硬的理解，并为心力衰竭治疗中针对这种僵硬提供了新的视角。