破骨细胞
骨吸收
兰克尔
骨重建
细胞生物学
骨质疏松症
骨重建期
吸收
巨噬细胞集落刺激因子
化学
免疫学
内科学
巨噬细胞
生物
内分泌学
医学
受体
生物化学
激活剂(遗传学)
体外
出处
期刊:STEMedicine
[Innovation Publishing House Pte. Ltd.]
日期:2020-09-03
卷期号:1 (4): e57-e57
被引量:36
标识
DOI:10.37175/stemedicine.v1i4.57
摘要
What we know about bone resorption has changed a lot in the last few decades. The osteoclast is the only cell to nibble and break down the bone, and in the formation and resorption of bone tissue, osteoclasts play an important role. Once the balance of bone formation and bone loss is out of control, diseases like osteopetrosis and osteoporosis occur. Bone resorption is a unique function of osteoblasts, which are multinucleated cells formed by the fusion of mononuclear progenitor cells of the monocyte/macrophage family. In the formation of osteoclasts, there are two main factors affecting this process, macrophage colony-stimulating factor (M-CSF) and ligand-activated receptor (RANKL) of nuclear factor kappa B (NF-κB). The identification of RANK-RANKL signaling and other classic signaling pathways such as Wnt and Notch, as the major signaling regulation in osteoclast differentiation, was a significant breakthrough in the field of osteoclastogenesis. In this review, we briefly describe the latest knowledge of osteoclast-induced bone resorption and cellular factors that regulate the activity of osteoclasts and cell fusion, for the purpose of understanding osteoclastogenesis and the development of drugs that enhance bone resorption to improve pathological bone diseases.
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