Living soft tissues appear to promote the development and maintenance of a preferred mechanical state within a defined tolerance around a so-called set point. This phenomenon is often referred to as mechanical homeostasis. In contradiction to the prominent role of mechanical homeostasis in various (patho)physiological processes, its underlying micromechanical mechanisms acting on the level of individual cells and fibers remain poorly understood, especially how these mechanisms on the microscale lead to what we macroscopically call mechanical homeostasis. Here, we present a novel computational framework based on the finite element method that is constructed bottom up, that is, it models key mechanobiological mechanisms such as actin cytoskeleton contraction and molecular clutch behavior of individual cells interacting with a reconstructed three-dimensional extracellular fiber matrix. The framework reproduces many experimental observations regarding mechanical homeostasis on short time scales (hours), in which the deposition and degradation of extracellular matrix can largely be neglected. This model can serve as a systematic tool for future in silico studies of the origin of the numerous still unexplained experimental observations about mechanical homeostasis.

活的软组织似乎在所谓的设定点周围的定义公差内促进优选机械状态的发展和维持。这种现象通常被称为机械稳态。与机械稳态在各种（病理）生理过程中的突出作用相反，其作用于单个细胞和纤维水平的潜在微机械机制仍然知之甚少，尤其是这些微观机制如何导致我们宏观上称为机械稳态的机制。在这里，我们提出了一种基于自下而上构建的有限元方法的新型计算框架，即 它模拟了关键的机械生物学机制，例如肌动蛋白细胞骨架收缩和单个细胞与重建的三维细胞外纤维基质相互作用的分子离合器行为。该框架再现了许多关于短时间尺度（小时）内机械稳态的实验观察结果，其中细胞外基质的沉积和降解在很大程度上可以忽略不计。该模型可以作为未来的系统工具在计算机上研究了许多关于机械稳态的仍然无法解释的实验观察的起源。