Han Duanyang, Zhang Peixun, Jiang Baoguo
Department of Orthopedics and Trauma, Peking University People's Hospital China.
Int J Clin Exp Med. 2015 Jan 15;8(1):1411-5. eCollection 2015.
Osteoporosis is an inflammatory bone disease affecting millions of population worldwide, which often cause increased fracture risks and prolonged fracture healing. Growing evidence suggests that IKK-NF-κB signaling exert inhibitory influence on MSCs osteogenic differentiation and bone formation. Moreover, enhance the fracture healing process in osteoporosis patient. In the current work, IKK-NF- κB differentiated osteoblasts. Thus, manipulating local inflammatory IKK-NF-κB signaling was also found to suppress the anabolic effect of signaling in osteoporotic related fracture emerge as a promising therapy to we hypothesized to use locally delivered IKK small molecule inhibitor to augment the impaired fracture healing ability in osteoporosis patient via enhancing both MSCs osteogenic differentiation and osteoblast function.
骨质疏松症是一种影响全球数百万人的炎性骨病，常导致骨折风险增加和骨折愈合时间延长。越来越多的证据表明，IKK-NF-κB信号通路对间充质干细胞（MSCs）的成骨分化和骨形成具有抑制作用。此外，该信号通路还会促进骨质疏松症患者的骨折愈合过程。在当前的研究中，IKK-NF-κB可分化成骨细胞。因此，我们发现操纵局部炎性IKK-NF-κB信号通路也可抑制骨质疏松症相关骨折中该信号通路的合成代谢作用，这有望成为一种治疗方法。我们假设通过增强MSCs的成骨分化和成骨细胞功能，使用局部递送的IKK小分子抑制剂来增强骨质疏松症患者受损的骨折愈合能力。
