The role of Ca2+-nfatc1 signaling and its modulation on osteoclastogenesis

Jung Yun Kang; Namju Kang; Yu Mi Yang; Jeong Hee Hong; Dong Min Shin

doi:10.3390/ijms21103646

The role of Ca²⁺-nfatc1 signaling and its modulation on osteoclastogenesis

Jung Yun Kang, Namju Kang, Yu Mi Yang, Jeong Hee Hong, Dong Min Shin

Department of Oral Biology

Research output: Contribution to journal › Review article › peer-review

33 Citations (Scopus)

Abstract

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.

Original language	English
Article number	3646
Journal	International journal of molecular sciences
Volume	21
Issue number	10
DOIs	https://doi.org/10.3390/ijms21103646
Publication status	Published - 2020 May 2

Bibliographical note

Funding Information:
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.)).

Publisher Copyright:
© 2020 by the authors. Licensee MDPI, Basel, Switzerland.

All Science Journal Classification (ASJC) codes

Catalysis
Molecular Biology
Spectroscopy
Computer Science Applications
Physical and Theoretical Chemistry
Organic Chemistry
Inorganic Chemistry

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10.3390/ijms21103646

Cite this

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title = "The role of Ca2+-nfatc1 signaling and its modulation on osteoclastogenesis",

abstract = "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.",

author = "Kang, {Jung Yun} and Namju Kang and Yang, {Yu Mi} and Hong, {Jeong Hee} and Shin, {Dong Min}",

note = "Funding Information: 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.)). Publisher Copyright: {\textcopyright} 2020 by the authors. Licensee MDPI, Basel, Switzerland.",

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AU - Yang, Yu Mi

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AU - Shin, Dong Min

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