Abstract
Introduction: Inflammatory bone resorption causes progressive joint destruction which ultimately leads to functional disability in rheumatoid arthritis (RA). The primary cell responsible for bone resorption is the osteoclast, which means it is a potential therapeutic target against bone destruction. In fact, experimental and clinical findings suggest that blockade of osteoclast differentiation and function is highly effective in inhibiting bone destruction in RA. Discussion and conclusion: In this report, we show several lines of experimental evidence which suggest that a variety of Ca2+ channels are essential in osteoclast differentiation and function, and present a hypothesis that modulation of Ca2+ channels is a highly effective therapeutic strategy in preventing osteoclast-induced structural damage in RA.
Original language | English |
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Pages (from-to) | 347-354 |
Number of pages | 8 |
Journal | Inflammation Research |
Volume | 65 |
Issue number | 5 |
DOIs | |
Publication status | Published - 2016 May 1 |
Externally published | Yes |
Bibliographical note
Funding Information:This study was supported by a Korea University Grant.
Publisher Copyright:
© 2016, Springer International Publishing.
Keywords
- Calcium channel
- Inflammation
- Osteoclast
- Rheumatoid arthritis
ASJC Scopus subject areas
- Immunology
- Pharmacology