Bone and Joint Research Unit, Instituto de Investigación Sanitaria, Fundación Jiménez Díaz, Universidad Autónoma de Madrid (UAM), Avenida de los Reyes Católicos 2, 28040 Madrid, Spain.
Bone and Joint Research Unit, Instituto de Investigación Sanitaria, Fundación Jiménez Díaz, Universidad Autónoma de Madrid (UAM), Avenida de los Reyes Católicos 2, 28040 Madrid, Spain.
Trends Endocrinol Metab. 2017 Oct;28(10):695-704. doi: 10.1016/j.tem.2017.06.003. Epub 2017 Jul 19.
Denosumab (Dmab) is a humanized monoclonal antibody that blocks RANKL (receptor activator for nuclear factor κB ligand), thereby exerting a potent bone antiresorptive action. Dmab treatment leads to a dramatic and sustained increase in bone mass through mechanisms that are currently under debate. It is also a matter of controversy whether this potent action of Dmab could lead to intrabone dystrophic mineralization. Recent research has uncovered a possible anabolic role of Dmab involving RANKL-dependent reverse signaling in osteoblasts, and that bone marrow adipocytes can modulate osteoclastogenesis through the production of RANKL. We comment here on potential pathways which might account for the anabolic action of Dmab. The impact of this proposed mechanism needs to be addressed in further research.
地舒单抗（Dmab）是一种人源化单克隆抗体，可阻断 RANKL（核因子 κB 配体受体激活剂），从而发挥强效的抗骨吸收作用。Dmab 通过目前正在讨论的机制导致骨量显著和持续增加。Dmab 的这种强效作用是否会导致骨内营养不良性矿化也存在争议。最近的研究揭示了 Dmab 的一种可能的合成代谢作用，涉及成骨细胞中 RANKL 依赖性反向信号转导，骨髓脂肪细胞可以通过产生 RANKL 来调节破骨细胞生成。我们在这里评论了可能解释 Dmab 合成代谢作用的潜在途径。需要进一步研究来解决这个拟议机制的影响。
