The increasing of intracellular calcium concentration is a fundamental process for mediating osteoclastogenesis, which is involved in osteoclastic bone resorption. Cytosolic calcium binds to calmodulin and subsequently activates calcineurin, leading to NFATc1 activation, a master transcription factor required for osteoclast differentiation. Targeting the various activation processes in osteoclastogenesis provides various therapeutic strategies for bone loss. Diverse compounds that modulate calcium signaling have been applied to regulate osteoclast differentiation and, subsequently, attenuate bone loss. Thus, in this review, we summarized the modulation of the NFATc1 pathway through various compounds that regulate calcium signaling and the calcium influx machinery. Furthermore, we addressed the involvement of transient receptor potential channels in osteoclastogenesis.
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Author Contributions: J.H.H., D.M.S., and J.Y.K. contributed to conception and design of manuscript; J.Y.K. drafted the article and revised it critically for important intellectual contents; N.K. and Y.-M.Y. collected data; J.H.H. and D.M.S. contributed to final approval of the version to be published. All authors are accountable for all aspects of the work. All authors have read and agreed to the published version of the manuscript Funding: This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korean Government MSIT (2019R1F1A1046785 (to J.H.H.), 2020R1A2C2003409 (to D.M.S.)).
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All Science Journal Classification (ASJC) codes
- Molecular Biology
- Computer Science Applications
- Physical and Theoretical Chemistry
- Organic Chemistry
- Inorganic Chemistry