The M-CSF receptor in osteoclasts and beyond.
Journal
Experimental & molecular medicine
ISSN: 2092-6413
Titre abrégé: Exp Mol Med
Pays: United States
ID NLM: 9607880
Informations de publication
Date de publication:
08 2020
08 2020
Historique:
received:
01
05
2020
accepted:
16
06
2020
revised:
15
06
2020
pubmed:
18
8
2020
medline:
11
8
2021
entrez:
18
8
2020
Statut:
ppublish
Résumé
Colony-stimulating factor 1 receptor (CSF1R, also known as c-FMS) is a receptor tyrosine kinase. Macrophage colony-stimulating factor (M-CSF) and IL-34 are ligands of CSF1R. CSF1R-mediated signaling is crucial for the survival, function, proliferation, and differentiation of myeloid lineage cells, including osteoclasts, monocytes/macrophages, microglia, Langerhans cells in the skin, and Paneth cells in the intestine. CSF1R also plays an important role in oocytes and trophoblastic cells in the female reproductive tract and in the maintenance and maturation of neural progenitor cells. Given that CSF1R is expressed in a wide range of myeloid cells, altered CSF1R signaling is implicated in inflammatory, neoplastic, and neurodegenerative diseases. Inhibiting CSF1R signaling through an inhibitory anti-CSF1R antibody or small molecule inhibitors that target the kinase activity of CSF1R has thus been a promising therapeutic strategy for those diseases. In this review, we cover the recent progress in our understanding of the various roles of CSF1R in osteoclasts and other myeloid cells, highlighting the therapeutic applications of CSF1R inhibitors in disease conditions.
Identifiants
pubmed: 32801364
doi: 10.1038/s12276-020-0484-z
pii: 10.1038/s12276-020-0484-z
pmc: PMC8080670
doi:
Substances chimiques
Ligands
0
Receptor, Macrophage Colony-Stimulating Factor
EC 2.7.10.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1239-1254Subventions
Organisme : NIAMS NIH HHS
ID : R01 AR069562
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR073156
Pays : United States
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