ArticleBone research2022
Sialylation of TLR2 initiates osteoclast fusion.
Article in Bone research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Targeting the Gut-Bone Axis with Prebiotics, Probiotics, Synbiotics, and Postbiotics: From Mechanistic Plausibility to Clinical Bone Outcomes.Nutrients · 2026Review
- Neutrophil-derived apoptotic bodies function as decoy signals to preserve bone integrity during infectious osteomyelitis.Bone research · 2026Article
- Breaking the immune "cold niche" in bone metastasis: core mechanisms of the multidimensional interwoven regulatory network and precision breakthrough strategies.Molecular cancer · 2026Review
- Estradiol regulates osteoclast sialylation via ST3Gal1 in postmenopausal osteoporosis.Bone research · 2026Article
- Beyond resorption: targeting osteoclast fusion and polarization to restore balanced bone remodeling.Frontiers in pharmacology · 2026Review
- Posaconazole mitigates α-amanitin-induced liver injury by inhibiting STT3B-mediated glycosylation and cellular uptake.Frontiers in pharmacology · 2026Article
- Article
- Fibroblast-derived NEU1 as a therapeutic target for improving cortical bone integrity and fracture healing.Theranostics · 2026Article
- Article
- Targeting Msx2 as a brake in the fusion fate of osteoclasts and an anabolic therapy in pre-clinical models of osteoporosis.Nature communications · 2025Article
- Trifunctional Sialylation-Based SF-ZIF@NA Hydrogel for Selective Osteoclast Inhibition and Enhanced Bone-Vessel Regeneration in Osteoporotic Bone Defects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Osteoclast-derived apoptotic bodies accelerate the pathological progression of osteoarthritis via disturbing subchondral bone remodeling.Journal of orthopaedic translation · 2025Article
- Inhibition of inflammatory osteoclasts accelerates callus remodeling in osteoporotic fractures by enhancing CGRPCell death and differentiation · 2024Article
- Mechanistic and Therapeutic Implications of Protein and Lipid Sialylation in Human Diseases.International journal of molecular sciences · 2024Review
- Review
- Proton-activated chloride channel increases endplate porosity and pain in a mouse spine degeneration model.The Journal of clinical investigation · 2024Article
- PCLAF induces bone marrow adipocyte senescence and contributes to skeletal aging.Bone research · 2024Article
- Regulation of Glycosylation in Bone Metabolism.International journal of molecular sciences · 2024Review
- The emerging role of osteoclasts in the treatment of bone metastases: rationale and recent clinical evidence.Frontiers in oncology · 2024Review
- Atsttrin regulates osteoblastogenesis and osteoclastogenesis through the TNFR pathway.Communications biology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The molecular control of osteoclast formation is still not clearly elucidated. Here, we show that a process of cell recognition mediated by Siglec15-TLR2 binding is indispensable and occurs prior to cell fusion in RANKL-mediated osteoclastogenesis. Siglec15 has been shown to regulate osteoclastic bone resorption. However, the receptor for Siglec15 has not been identified, and the signaling mechanism involving Siglec15 in osteoclast function remains unclear. We found that Siglec15 bound sialylated TLR2 as its receptor and that the binding of sialylated TLR2 to Siglec15 in macrophages committed to the osteoclast-lineage initiated cell fusion for osteoclast formation, in which sialic acid was transferred by the sialyltransferase ST3Gal1. Interestingly, the expression of Siglec15 in macrophages was activated by M-CSF, whereas ST3Gal1 expression was induced by RANKL. Both Siglec15-specific deletion in macrophages and intrafemoral injection of sialidase abrogated cell recognition and reduced subsequent cell fusion for the formation of osteoclasts, resulting in increased bone formation in mice. Thus, our results reveal that cell recognition mediated by the binding of sialylated TLR2 to Siglec15 initiates cell fusion for osteoclast formation.
Identifiers
What OpenQuestion holds
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.