The role of NFAT in osteoclast formation

TAKAYANAGI, HIROSHI

doi:10.1196/annals.1402.071

Cited by 442Bone Metabolism and DiseasesSignaling Pathways in DiseaseNuclear Receptors and Signaling

The role of NFAT in osteoclast formation

TAKAYANAGI, HIROSHI·2007·Annals of the New York Academy of Sciences

DOI 10.1196/annals.1402.071

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Abstract

Osteoclasts are cells of monocyte-macrophage origin that degrade bone matrix. Receptor activator of NF-kappaB ligand (RANKL) induces osteoclast formation in the presence of macrophage-colony-stimulating factor (M-CSF) and costimulatory signals. RANKL induces activation of the TNF receptor-associated factor 6 (TRAF6) and c-Fos pathways, which lead to the osteoclast-specific event, that is, autoamplification of nuclear factor of activated T cells (NFAT)c1, the master transcription factor for osteoclast differentiation. Autoamplification of NFATc1 is dependent on the calcium signaling of immunoglobulin-like receptors associated with immunoreceptor tyrosine-based activation motif (ITAM)-harboring adaptors. In addition to the calcineurin-NFATc1 axis, calcium signaling activates the calmodulin-dependent kinase pathway, which also plays a critical role in osteoclast formation. Such advances in the understanding of the molecular mechanism of osteoclast differentiation are expected to lead to novel therapeutic approaches to bone diseases.

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The calcineurin pathway is a key costimulatory pathway of NFATc1 and an important signaling component of a number of immune cell receptors.
“This activates cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) and the calcineurin pathway [21,24,25,27], a key costimulatory pathway of NFATc1 [21,23] and an important signaling component of a number of immune cell receptors [28] (Figure 4 and Figure 5).”
From Osteoclasts and Microgravity (2020) · cites this paper as [25]
NFATc1 binds to its own promoter, switching on an epigenetically controlled autoregulatory cycle that permits efficient induction of TRAP, cathepsin K, DC-STAMP, and ATP6v0d2.
“NFATc1 binds to its own promoter, switching on an epigenetically controlled autoregulatory cycle that permits efficient induction of the osteoclast-specific genes, tartrate-resistant acid phosphatase (TRAP), cathepsin K, as well as the fusion-specific genes, dendritic cell-specific transmembrane protein (DC-STAMP) and ATPase H+ transporting V0 subunit D2 (ATP6v0d2) [20,25,26] (Figure 3).”
From Osteoclasts and Microgravity (2020) · cites this paper as [25]

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Authors: TAKAYANAGI, H.
Affiliations: Tokyo Medical and Dental University (JP)
Corresponding author: TAKAYANAGI, HIROSHI
ORCID: TAKAYANAGI, HIROSHI
Venue: Annals of the New York Academy of Sciences
Publisher: Wiley
Published: 2007-11
Volume: 1116
Issue: 1
Pages: 227-237
ISSN: 0077-8923 (ISSN-L)
1749-6632
DOI: 10.1196/annals.1402.071
OpenAlex: W1975505424
Cited by: 442
References: 36
Citations by year: 2026: 6 · 2025: 16 · 2024: 16 · 2023: 21 · 2022: 23 · 2021: 21 · 2020: 33 · 2019: 35 · 2018: 34 · 2017: 28 · 2016: 31 · 2015: 38 · 2014: 19 · 2013: 22 · 2012: 29
FWCI: 1.13
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 42 d)
Locations: Annals of the New York Academy of Sciences (publishedVersion)
PubMed (publishedVersion)
Funders: Kanae Foundation for the Promotion of Medical Science
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
Keywords: osteoclastogenesis, NFATc1, RANKL, TRAF6, c-fos, calcineurin, calcium signaling, calcium/calmodulin-dependent protein kinase, ITAM, macrophage colony-stimulating factor, bone resorption, bone disease
MeSH terms: Animals, Humans, Osteoclasts, Transcription, Genetic, Signal Transduction, NFATC Transcription Factors, RANK Ligand

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The role of NFAT in osteoclast formation

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