巩膜重塑、弹性承载力降低是近视眼轴延长的最终环节，然而机制不完全清晰。最近，本课题组发现，介导力学生物学信号转导的Integrinα2β1在形觉剥夺近视小鼠巩膜组织中显著下调，且与近视度数相关，但作用不明。为此，本课题对近视动物模型和培养于3D软性基质的细胞模型，运用基因敲除及重组技术，首先研究下调的Integrinα2β1是否通过RhoA调节YAP/TAZ使下游的胶原代谢相关因子表达减少，导致巩膜弹性模量下降、眼轴延长，其次阐明Integrinα2β1是否通过胞浆骨架蛋白(F-actin)重构影响细胞收缩力并调控YAP/TAZ起作用，进而，以Integrinα2β1-YAP/TAZ为靶标进行干预，揭示其可能是近视治疗的有效靶点。迄今，这些研究在国际上尚属空白，其预期的研究结果可能丰富人们对近视巩膜重塑中力学生物学机制的认识，为近视防治提供理论和实验依据，具有重要的理论和现实意义。

Scleral remodeling and its elasticity decrease are the final processes of the axial length elongation in myopia. However, the mechanism of these processes still remains unknown. Recently, our study group found that Integrinα2β1, a protein that mediating mechano-biological signaling transduction is significantly down-regulated in the sclera of form deprivation myopia (FDM) mice, and its change is correlated with myopic degree. But the role of Integrinα2β1 is unclear. Therefore, we apply gene knock-out and recombination technique in mice FDM and 3-D soft substratum cell culture model, firstly, to elucidate if Integrinα2β1 can regulate YAP/TAZ pathway and its downstream collagen metabolic molecular by RhoA pathway, which lead to elasticity modulus decrease and scleral axial length elongation; Secondly, if down-regulated Integrinα2β1 can influence cell-mediated collagen gel’s contraction and YAP/TAZ by regulating the reconstruction of cellular skeleton protein (F-actin). Then, we target Integrinα2β1-YAP/TAZ for intervention, to reveal if it could be a potential therapeutic target in myopic control. To the best of our knowledge, no related research has been published by now. Our study may enrich the perspective in biomechanics of scleral remodeling, and provide with both theoretical and experimental evidence for prevention and treatment in myopia.