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Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
Published on: March 18, 2019
Recent advances in osteoclast biology
Takehito Ono1,2, Tomoki Nakashima3,4
1Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Yushima 1-5-45, Bunkyo-ku, Tokyo, 113-8549, Japan. ono.csi@tmd.ac.jp.
Bone remodeling involves osteoclasts and osteoblasts. RANKL/RANK signaling is crucial for osteoclast formation, and its dysregulation causes bone diseases like osteoporosis.
Area of Science:
- Bone biology and skeletal physiology.
Background:
- Bone tissue maintains locomotion, protection, hematopoiesis, and mineral homeostasis through continuous resorption and formation.
- Osteoclasts, multinucleated cells derived from monocytes/macrophages, are responsible for bone resorption.
- Osteoclast differentiation is regulated by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-κB ligand (RANKL).
Purpose of the Study:
- To review current findings on osteoclast biology.
- To summarize the role of RANKL/RANK signaling in osteoclastogenesis.
- To highlight the implications of RANKL signaling dysregulation in bone diseases.
Main Methods:
- This review synthesizes existing research on osteoclast differentiation and function.
- It examines the molecular mechanisms of RANKL/RANK signaling pathway.
- Literature search and analysis of studies on bone remodeling and related diseases were performed.
Main Results:
- RANKL binding to its receptor RANK initiates signaling cascades, notably activating NFATc1, the key regulator of osteoclastogenesis.
- Various cell types express RANKL, influencing osteoclast formation based on biological context.
- Aberrant RANKL signaling is implicated in skeletal pathologies.
Conclusions:
- Osteoclast activity, regulated by RANKL/RANK signaling, is fundamental to bone homeostasis.
- Understanding this pathway is critical for addressing bone diseases such as osteoporosis and osteopetrosis.
- Further research into RANKL/RANK signaling holds therapeutic potential for skeletal disorders.
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