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Recent advances in osteoclast biology.

Authors
  • Ono, Takehito1, 2
  • Nakashima, Tomoki3, 4
  • 1 Department 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. [email protected] , (Japan)
  • 2 Core Research for Evolutional Science and Technology (CREST), Japan Agency for Medical Research and Development (AMED), Yushima 1-5-45, Bunkyo-ku, Tokyo, 113-8549, Japan. [email protected] , (Japan)
  • 3 Department 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. , (Japan)
  • 4 Core Research for Evolutional Science and Technology (CREST), Japan Agency for Medical Research and Development (AMED), Yushima 1-5-45, Bunkyo-ku, Tokyo, 113-8549, Japan. , (Japan)
Type
Published Article
Journal
Histochemistry and cell biology
Publication Date
Apr 01, 2018
Volume
149
Issue
4
Pages
325–341
Identifiers
DOI: 10.1007/s00418-018-1636-2
PMID: 29392395
Source
Medline
Keywords
License
Unknown

Abstract

The bone is an essential organ for locomotion and protection of the body, as well as hematopoiesis and mineral homeostasis. In order to exert these functions throughout life, bone tissue undergoes a repeating cycle of osteoclastic bone resorption and osteoblastic bone formation. The osteoclast is a large, multinucleated cell that is differentiated from monocyte/macrophage lineage cells by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-κB ligand (RANKL). RANKL transduces its signal through the signaling receptor, RANK. RANKL/RANK signaling activates NFATc1, the master regulator of osteoclastogenesis, to induce osteoclastogenic gene expression. Many types of cells express RANKL to support osteoclastogenesis depending on the biological context and the dysregulation of RANKL signaling leads to bone diseases such as osteoporosis and osteopetrosis. This review outlines the findings on osteoclast and RANKL/RANK signaling that have accumulated to date.

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