The ability of biological systems to withstand and recover from various disruptions, such as spontaneous genetic mutations and environmental damage, largely relies on intricate feedback mechanisms. We theoretically study the mechanical response of an epithelial tissue facing damage in the form of a circular wound. Our model describes a feedback loop between the generation of active forces in the actomyosin and tissue mechanics, described by the vertex model. While the exact dynamics of wound closure may be influenced by several biophysical mechanisms that interplay in a nontrivial way, our findings suggest that the closure may initiate as an active instability, triggered by a reduced myosin turnover rate at the wound’s perimeter. We explore the interplay between myosin dynamics and the elastic properties of the tissue, elucidating their collective role in determining a wound’s loss of stability, leading to the initiation of the closure process.

中文翻译：

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由荷链处的活动性不稳定开始上皮伤口闭合


生物系统承受各种干扰（例如自发性基因突变和环境破坏）并从中恢复的能力在很大程度上取决于复杂的反馈机制。我们从理论上研究了以圆形伤口形式面临损伤的上皮组织的机械反应。我们的模型描述了肌动球蛋白中作用力的产生和组织力学之间的反馈回路，由顶点模型描述。虽然伤口闭合的确切动力学可能受到几种生物物理机制的影响，这些机制以非平凡的方式相互作用，但我们的研究结果表明，闭合可能以主动不稳定的形式开始，由伤口周边的肌球蛋白周转率降低触发。我们探讨了肌球蛋白动力学与组织弹性特性之间的相互作用，阐明了它们在决定伤口失去稳定性、导致闭合过程开始方面的集体作用。