Role of the Interaction of Tumor Necrosis Factor-α and Tumor Necrosis Factor Receptors 1 and 2 in Bone-Related Cells.
TNF receptor-1
TNF receptor-2
TNF-α
osteoblast
osteoclast
osteocyte
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
27 Jan 2022
27 Jan 2022
Historique:
received:
29
12
2021
revised:
24
01
2022
accepted:
26
01
2022
entrez:
15
2
2022
pubmed:
16
2
2022
medline:
15
3
2022
Statut:
epublish
Résumé
Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine expressed by macrophages, monocytes, and T cells, and its expression is triggered by the immune system in response to pathogens and their products, such as endotoxins. TNF-α plays an important role in host defense by inducing inflammatory reactions such as phagocytes and cytocidal systems activation. TNF-α also plays an important role in bone metabolism and is associated with inflammatory bone diseases. TNF-α binds to two cell surface receptors, the 55kDa TNF receptor-1 (TNFR1) and the 75kDa TNF receptor-2 (TNFR2). Bone is in a constant state of turnover; it is continuously degraded and built via the process of bone remodeling, which results from the regulated balance between bone-resorbing osteoclasts, bone-forming osteoblasts, and the mechanosensory cell type osteocytes. Precise interactions between these cells maintain skeletal homeostasis. Studies have shown that TNF-α affects bone-related cells via TNFRs. Signaling through either receptor results in different outcomes in different cell types as well as in the same cell type. This review summarizes and discusses current research on the TNF-α and TNFR interaction and its role in bone-related cells.
Identifiants
pubmed: 35163403
pii: ijms23031481
doi: 10.3390/ijms23031481
pmc: PMC8835906
pii:
doi:
Substances chimiques
Receptors, Tumor Necrosis Factor, Type I
0
Receptors, Tumor Necrosis Factor, Type II
0
TNFRSF1A protein, human
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Japan Society for the Promotion of Science
ID : 19K10397
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