Liedert A, Schinke T, Ignatius A, Amling M
Institute of Orthopedic Research and Biomechanics, Center of Musculoskeletal Research, University of Ulm, Ulm, Germany.
Br J Pharmacol. 2014 Feb;171(4):870-8. doi: 10.1111/bph.12412.
Bone tissue is subjected to continuous remodelling, replacing old or damaged bone throughout life. In bone remodelling, the coordinated activities of bone-forming osteoblasts and bone-resorbing osteoclasts ensure the maintenance of bone mass and strength. In early life, the balance of these cellular activities is tightly regulated by various factors, including systemic hormones, the mechanical environment and locally released growth factors. Age-related changes in the activity of these factors in bone remodelling can result in diseases with low bone mass, such as osteoporosis. Osteoporosis is a systemic and age-related skeletal disease characterized by low bone mass and structural degeneration of bone tissue, predisposing the patient to an increased fracture risk. The growth factor midkine (Mdk) plays a key role in bone remodelling and it is expressed during bone formation and fracture repair. Using a mouse deficient in Mdk, our group have identified this protein as a negative regulator of bone formation and mechanically induced bone remodelling. Thus, specific Mdk antagonists might represent a therapeutic option for diseases characterized by low bone mass, such as osteoporosis.
This article is part of a themed section on Midkine. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-4.
骨组织会持续进行重塑，在一生中不断替换老旧或受损的骨骼。在骨重塑过程中，成骨的成骨细胞和破骨的破骨细胞的协同活动确保了骨量和骨强度的维持。在生命早期，这些细胞活动的平衡受到多种因素的严格调控，包括全身性激素、力学环境和局部释放的生长因子。这些因素在骨重塑活动中与年龄相关的变化可能会导致低骨量疾病，如骨质疏松症。骨质疏松症是一种与年龄相关的全身性骨骼疾病，其特征是骨量低和骨组织结构退变，使患者骨折风险增加。生长因子中期因子（Mdk）在骨重塑中起关键作用，并且在骨形成和骨折修复过程中表达。利用Mdk基因敲除小鼠，我们团队已确定该蛋白是骨形成和机械诱导骨重塑的负调节因子。因此，特异性Mdk拮抗剂可能是治疗以低骨量为特征的疾病（如骨质疏松症）的一种治疗选择。
本文是关于中期因子的主题章节的一部分。若要查看本章节的其他文章，请访问http://dx.doi.org/10.1111/bph.2014.171.issue-4。
