深入研究破骨细胞的分化及骨吸收功能的调控机制，对于骨质疏松、关节炎和骨肿瘤等多种骨代谢性疾病的预防和治疗具有重要意义。课题组前期发现cyclin G2参与骨质疏松发生发展，证实cyclin G2在成骨细胞中负性调控经典Wnt信号通路，提示其对破骨细胞的分化和功能可能具有调控作用。另外，我们筛选到的cyclin G2结合蛋白提示其可能通过调控细胞骨架动态重组，影响破骨细胞迁移和骨吸收功能。本项目利用前期已经构建的Ccng2-/-小鼠，获得cyclin G2基因敲除的破骨前体细胞和破骨细胞，用于研究cyclin G2调控破骨细胞分化、凋亡和骨吸收功能的调控作用，阐明其分子机制并在小鼠体内进行验证。通过骨质疏松疾病动物模型，明确cyclin G2调控破骨细胞分化和骨吸收在骨质疏松中的作用和分子机制，丰富破骨细胞分化和骨吸收调控理论，为骨代谢性疾病的预防和治疗提供新靶点和新方向。

Explore the underlying mechanisms of osteoclast differentiation and bone resorption are important for the prevention and treatment of bone metabolic diseases, such as osteoporosis, arthritis and tumor induced bone resorption. Our previous research found that cyclin G2 regulated osteogenesis is involved in the development of osteoporosis through inhibition of canonical Wnt/β-catenin signaling pathway, indicated the potential function of cyclin G2 on osteoclast differentiation and bone resorption. In addition, we screened cyclin G2 binding protein using hybrid systems, suggesting that it may affect the dynamic reorganization of osteoclast migration and bone resorption by regulating cytoskeleton. We also generated cyclin G2 knock out mice for future investigation. In this program, cyclin G2 knockout osteoclast precursor cells and osteoclasts generated from Ccng2-/ - mice was used to explore the regulation of cyclin G2 in osteoclast differentiation, apoptosis and the regulation of bone resorption, and to clarify the molecular mechanisms in vivo.