ArticleJournal of orthopaedic translation2024
The CD163/TWEAK/Fn14 axis: A potential therapeutic target for alleviating inflammatory bone loss.
Article in Journal of orthopaedic translation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Expression of Molecular Markers Associated with Tenosynovial Giant Cell Tumours and Bone Destruction: A Systematic Review.Journal of clinical medicine · 2026Review
- TWEAK modulates the characteristics of periodontal ligament stem cells via the Fn14/NF‑κB pathway.International journal of molecular medicine · 2026Article
- CD163 Expression Protects Against Early Hepatic Steatosis in Western Diet-Fed Male Mice.Gastro hep advances · 2026Article
- Long-term Western diet feeding impairs hepatic vitamin D metabolism and promotes bone loss in mice.EXCLI journal · 2026Article
- Baicalin Alleviates Piglet Immunosuppression Induced byBiomolecules · 2025Article
- New developments in osteoporosis, osteoarthritis and soft tissue repair.Journal of orthopaedic translation · 2024Article
Corrections and comments
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Osteoclast (OC) over-activation is an important cause of bone loss that is strongly correlated with inflammation. Although the CD163/TWEAK/Fn14 axis has been implicated in several inflammatory pathologies, its contributions to inflammatory bone loss remain poorly understood. This study aimed to evaluate the interaction of the CD163/TWEAK/Fn14 axis with OC in inflammatory bone loss. Methods: To assess the role of CD163 in bone homeostasis, we characterized the bone phenotypes of CD163-deficient mice and their wild-type littermates. CD163 and TWEAK levels were evaluated in the bone marrow of mice with LPS-induced bone loss and individuals with rheumatoid arthritis (RA). Bone mass changes were assessed using uCT and histology following supplementation with recombinant mouse CD163 protein (rCD163) or blockade of TWEAK/Fn14 signaling in CD163-deficient mice and mice with LPS-induced bone loss. The impact of CD163/TWEAK on OC differentiation and bone resorption capacity was analyzed Results: CD163 deficiency caused decreased bone mass and increased OC abundance. Lower CD163 expression and higher TWEAK expression were observed in the bone marrow of mice with LPS-induced bone loss and individuals with RA. TWEAK, mainly derived from CD68 Conclusion: Our findings suggest that the CD163/TWEAK/Fn14 axis is a potential therapeutic target for inflammatory bone loss by regulating osteoclastogenesis.
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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 Socratic graph.