生物力学微环境通过调控细胞迁移促进创面修复的研究进展

Research advances on the biomechanical micro-environment facilitated wound repair through the regulation of cell migration

生物力学微环境是指细胞外的力学微环境中的多种力学信号,其会随着时间和空间发生相应的变化,在细胞迁移、增殖和分化等组织学改变中起着重要作用,并可进一步影响创面愈合。创面愈合是一个复杂的病理生理过程,其中细胞能否高效并快速地往创面中心迁移是影响创面愈合的重要因素之一。既往研究表明,生物力学微环境不仅可诱导细胞进行定向迁移,还可提高细胞的迁移速度。在复杂的自然环境中,细胞采取多种迁移模式,且受局部肌球蛋白收缩性和细胞外微环境等特殊模式支配;除了克服细胞外屏障,细胞还需通过局部物理机械力和信号与邻近的细胞和组织进行相互作用完成迁移,从而加速创面愈合。因此,近年来国内外学者都在积极研发各种基于改善生物力学微环境的生物材料,以期进一步促进细胞迁移从而加速创面愈合。本文就近年来生物力学微环境通过调控细胞迁移促进创面修复及相关生物材料开发的研究进展进行综述。

Biomechanical microenvironment refers to a variety of mechanical signals in the extracellular mechanical microenvironment,which will change correspondingly with time and space.It plays an important role in histological changes such as cell migration,proliferation,and differentiation,and can further affect wound healing.Wound healing is a complex pathophysiological process,and one of the important factors that affects wound healing is whether the cells can efficiently and quickly migrate to the wound center or not.Previous studies have shown that biomechanical microenvironment can not only induce the directional migration of cells,but also improve the migration rate of cells.In the complex natural environment,cells adopt various migration patterns and are dominated by special patterns such as local myosin contractility and extracellular microenvironment.In addition to overcoming the extracellular barrier,cells also need to interact with neighboring cells and tissue through local physical and mechanical forces and signals to complete migration and thus accelerate wound healing.Therefore,in recent years,scholars at home and abroad have been actively developing biological materials based on improving biomechanical microenvironment in order to further promote cell migration and thus accelerate wound healing.This paper reviews the recent research advances on the role of biomechanical environment in wound healing promotion via the regulating of cell migration and the development of related biomaterials.