肌腱和韧带止点损伤修复后，骨-肌腱结合部（Bone-Tendon Junction，BTJ）仅以瘢痕连接愈合，难以恢复原本的软骨性连接，有损其传递和缓冲应力的功能，再损伤率高。隶属于BMP家族的CDMP1、2、3可促成纤维细胞向软骨细胞转化,而Tob蛋白及其相关信号通路密切参与此过程，但其具体参与细节尚不得而知。 在此基础上，本研究拟构建大鼠BTJ损伤修复模型，在体研究Tob蛋白及其相关信号通路在其愈合过程与组织形态重塑的相关性；分别在愈合与重塑的不同时期，用针对Tob蛋白、ISmad-6、7的siRNA和针对p90rsk-1的质粒转染BTJ，促进成纤维细胞向软骨细胞转化的同时，测量有关基因通路（BMP/Smad通路，ras/MAPK通路）信号蛋白水平的改变。 本研究可望阐明Tob蛋白及其相关信号通路对BTJ瘢痕愈合与重塑的调节机制，为基因治疗促进BTJ处组织形态重塑提供依。

Tendon and ligament repair, bone tendon junction (Bone-Tendon Junction, BTJ) connected only to scar healing, difficult to restore cartilage of the original connection, damage its stress transfer and buffer function, high rate of reperfusion injury.Belonging to the BMP family CDMP1, 2, 3 can promote fibroblast into cartilage cells, and Tob protein and its related signal pathway was closely involved in this process.On this basis, this study is to construct a model of BTJ injury in rats in vivo, Tob Protein and its related signaling pathway in the healing process and tissue remodeling correlation; at different times of healing and remodeling, the Tob protein, ISmad-6, 7 siRNA and targeting p90rsk-1 plasmids were transfected into BTJ fibroblasts, promote chondrogenesis, changes and biomechanical cells and extracellular matrix were observed after regulation the BTJ, in order to promote cartilage junction remodeling, improve its ultimate load and strength. This study will clarify the Tob protein and its related signal pathway on BTJ scar healing and regulation mechanism of remodeling, gene therapy for promoting BTJ tissue remodeling and provide the basis.