OPG/RANKL/RANK信号通路在骨巨细胞瘤发病机制中的作用.

BACKGROUND: Studies have shown that osteoprotegerin/receptor activator of nuclear factor κB ligand/nuclear factor κB receptor activator (OPG/RANKL/RANK) signaling pathway has a certain correlation with the pathogenesis of giant-cell tumor. Controlling the OPG/RANKL/RANK signaling pathway to affect the interaction between osteoblasts and osteoclasts can play a certain therapeutic role in giant-cell tumor of bone. OBJECTIVE: Ton introduce the relationship between the OPG/RANKL/RANK signaling pathway and the pathogenesis of giant-cell tumor of bone, and to summarize and discuss the new advances of the OPG/RANKL/RANK signaling pathway in the pathogenesis of giant-cell tumor of bone. METHODS: PubMed, Web of Science, and WanFang databases were searched for relevant articles published from 2001 to 2019 using the keywords of “OPG/RANKL/RANK, giant cell tumor of bone, pathogenesis, signal pathway, bone metabolism" in English and Chinese, respectively. A total of 53 articles were finally included for analysis and discussion after removal of old and repeated literatures. RESULTS AND CONCLUSION: OPG inhibits the proliferation and differentiation of osteoclasts, reduces the activity of mature osteoclasts, and blocks the binding of RANKL to RANK. RANKL binds to RANK on the surface of osteoclast progenitor cells to promote the differentiation and proliferation of osteoclast progenitor cells, thus accelerating osteoclast progression. After binding to RANKL receptor, RANKL activates signal factors such as nuclear factor-κB to promote the proliferation, differentiation and activation of osteoclasts, and to regulate the transcription and expression of related genes. Therefore, the OPG/RANKL/RANK is associated with the pathogenesis of giant-cell tumor. [ABSTRACT FROM AUTHOR]