The Role of TAK1 in RANKL-Induced Osteoclastogenesis

Bone remodelling is generally a dynamic process orchestrated by bone-resorbing osteoclasts and bone-forming osteoblasts. Osteoclasts are the only cell type capable of bone resorption to maintain bone homeostasis in the human body. However, excessive osteoclastogenesis can lead to osteolytic diseases...

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Bibliographic Details
Published in:Calcified tissue international 2022-07, Vol.111 (1), p.1-12
Main Authors: Jianwei, Wu, Ye, Tian, Hongwei, Wang, Dachuan, Li, Fei, Zou, Jianyuan, Jiang, Hongli, Wang
Format: Article
Language:English
Subjects:
Biochemistry
Biomedical and Life Sciences
Bone remodeling
Bone resorption
Bone turnover
Cell Biology
Cell survival
Endocrinology
Homeostasis
Intracellular signalling
Kinases
Life Sciences
MAP kinase
NF-κB protein
Orthopedics
Osteoclastogenesis
Osteoclasts
Osteolysis
Osteoporosis
Protein kinase
Review Article
Signal transduction
TAK1 protein
TRANCE protein
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Summary:Bone remodelling is generally a dynamic process orchestrated by bone-resorbing osteoclasts and bone-forming osteoblasts. Osteoclasts are the only cell type capable of bone resorption to maintain bone homeostasis in the human body. However, excessive osteoclastogenesis can lead to osteolytic diseases. The receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL) has been widely considered to be an important modulator of osteoclastogenesis thereby participating in the pathogenesis of osteolytic diseases. Transforming growth factor β-activated kinase 1 (TAK1), a member of the mitogen-activated protein kinase kinase kinase family, is an important intracellular molecule that regulates multiple signalling pathways, such as NF-κB and mitogen-activated protein kinase to mediate multiple physiological processes, including cell survival, inflammation, and tumourigenesis. Furthermore, increasing evidence has demonstrated that TAK1 is intimately involved in RANKL-induced osteoclastogenesis. Moreover, several detailed mechanisms by which TAK1 regulates RANKL-induced osteoclastogenesis have been clarified, and some potential approaches targeting TAK1 for the treatment of osteolytic diseases have emerged. In this review, we discuss how TAK1 functions in RANKL-mediated signalling pathways and highlight the significant role of TAK1 in RANKL-induced osteoclastogenesis. In addition, we discuss the potential clinical implications of TAK1 inhibitors for the treatment of osteolytic diseases.
ISSN:1432-0827
0171-967X
1432-0827
DOI:10.1007/s00223-022-00967-z