ReviewCalcified tissue international2022
The Role of TAK1 in RANKL-Induced Osteoclastogenesis.
Review in Calcified tissue international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- [Imaging assessment and treatment of Charcot arthropathy of the shoulder assisted by NGH classification].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Metabolic and neuroimmune control of rheumatoid arthritis: therapeutic implications of FXR and α7-nAChR axes.Inflammopharmacology · 2026Review
- Significant association of RANKL polymorphisms with bone metastasis among patients with breast cancer.Frontiers in oncology · 2026Article
- Dual regulation of phaseol on osteoclast formation and osteoblast differentiation by targeting TAK1 kinase for osteoporosis treatment.Journal of advanced research · 2025Article
- Clustered peptide regulating the multivalent interaction between RANK and TRAF6 inhibits osteoclastogenesis by fine-tuning signals.Communications biology · 2025Article
- TRAF1 promotes osteoclastogenesis by enhancing metabolic adaptation to oxidative phosphorylation in an AKT-dependent manner.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Mechanisms of isorhamnetin inhibition of osteoclast differentiation: insights from molecular dynamics simulations andFrontiers in pharmacology · 2025Article
- Quercetin in Osteoporosis Treatment: A Comprehensive Review of Its Mechanisms and Therapeutic Potential.Current osteoporosis reports · 2024Review
- LncRNA-mediated cartilage homeostasis in osteoarthritis: a narrative review.Frontiers in medicine · 2024Review
- Cinchonine: A Versatile Pharmacological Agent Derived from Natural Cinchona Alkaloids.Current topics in medicinal chemistry · 2024Review
- Extracellular vesicles derived from M1 macrophages enhance rat midpalatal suture expansion by promoting initial bone turnover and inflammation.Progress in orthodontics · 2023Article
- Growth charts for Marfan syndrome in the Netherlands and analysis of genotype-phenotype relationships.American journal of medical genetics. Part A · 2023Article
- Recent advances of the mammalian target of rapamycin signaling in mesenchymal stem cells.Frontiers in genetics · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.