Division of Bone and Mineral Diseases, Department of Medicine, Washington University School of Medicine, St Louis, MO, USA.
Cell Res. 2011 Jan;21(1):169-82. doi: 10.1038/cr.2010.159. Epub 2010 Nov 16.
Since the discovery that deletion of the NF-κB subunits p50 and p52 causes osteopetrosis in mice, there has been considerable interest in the role of NF-κB signaling in bone. NF-κB controls the differentiation or activity of the major skeletal cell types - osteoclasts, osteoblasts, osteocytes and chondrocytes. However, with five NF-κB subunits and two distinct activation pathways, not all NF-κB signals lead to the same physiologic responses. In this review, we will describe the roles of various NF-κB proteins in basal bone homeostasis and disease states, and explore how NF-κB inhibition might be utilized therapeutically.
自发现 NF-κB 亚基 p50 和 p52 的缺失会导致小鼠发生骨质硬化症以来,人们对 NF-κB 信号在骨骼中的作用产生了浓厚的兴趣。NF-κB 控制着主要骨骼细胞类型——破骨细胞、成骨细胞、骨细胞和软骨细胞的分化或活性。然而,由于有五个 NF-κB 亚基和两种不同的激活途径,并非所有 NF-κB 信号都导致相同的生理反应。在这篇综述中,我们将描述各种 NF-κB 蛋白在基础骨稳态和疾病状态中的作用,并探讨 NF-κB 抑制如何在治疗中得到应用。