ArticleInternational journal of molecular sciences2021
GPR120 Inhibits RANKL-Induced Osteoclast Formation and Resorption by Attenuating Reactive Oxygen Species Production in RAW264.7 Murine Macrophages.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Chrysin Exhibits Bone-Protective Effects Through Osteoclastogenesis Inhibition: In Vitro and In Vivo Evaluation in RAW 264.7 Murine Macrophages and Sprague-Dawley Rats.Molecular nutrition & food research · 2026Article
- Fatty Acid-Sensing G Protein-Coupled Receptors in Skeletal Metabolism.Journal of bone metabolism · 2026Article
- Progress on Omega-3 fatty acids for the comprehensive and targeted treatment of spinal cord injury.Bone research · 2026Review
- Omega-3 PUFAs in musculoskeletal health and sports medicine: from molecular pathways to precision nutrition strategies.Frontiers in nutrition · 2026Review
- New NaBMC chemistry · 2025Article
- Docosahexaenoic Acid Inhibits Osteoclastogenesis via FFAR4-Mediated Regulation of Inflammatory Cytokines.Molecules (Basel, Switzerland) · 2025Review
- Sinensetin serves as an AMPK activator to inhibit RANKL-induced osteoclastogenesis via osteoclast cytoskeleton reorganization.Journal of translational medicine · 2025Article
- The function of GPCRs in different bone cells.International journal of biological sciences · 2025Review
- Trained immunity of synovial macrophages is associated with exacerbated joint inflammation and damage after Staphylococcus aureus infection.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Advances in the Pathogenesis of Steroid-Associated Osteonecrosis of the Femoral Head.Biomolecules · 2024Review
- Crosstalk between Lipid Metabolism and Bone Homeostasis: Exploring Intricate Signaling Relationships.Research (Washington, D.C.) · 2024Article
- CB2 regulates oxidative stress and osteoclastogenesis through NOX1-dependent signaling pathway in titanium particle-induced osteolysis.Cell death discovery · 2023Article
- Recent Advance in Regulatory Effect of GRP120 on Bone Metabolism.Aging and disease · 2023Review
- The Potential Roles of Ferroptosis in Pathophysiology and Treatment of Musculoskeletal Diseases-Opportunities, Challenges, and Perspectives.Journal of clinical medicine · 2023Review
- Periplaneta Americana extract inhibits osteoclastic differentiation in vitro.Cell proliferation · 2023Article
- Changes in Metabolism and Mitochondrial Bioenergetics during Polyethylene-Induced Osteoclastogenesis.International journal of molecular sciences · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Osteoclasts are large, multinucleated cells that are responsible for the resorption of bone. Bone degenerative diseases, such as osteoporosis, are characterized by overactive osteoclasts. Receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL) binding to its receptor on osteoclast precursors will trigger osteoclast formation and resorption. The production of reactive oxygen species (ROS) is known to play a crucial role in RANKL-induced osteoclast formation and resorption. G-protein coupled receptor 120 (GPR120) signalling has been shown to affect osteoclast formation, but the exact mechanisms of action require further investigation. RAW264.7 murine macrophages were seeded into culture plates and exposed to the GPR120 agonist, TUG-891, at varying concentrations (20-100 µM) and RANKL to induce osteoclast formation. TUG-891 was shown to inhibit osteoclast formation and resorption without affecting cell viability in RAW264.7 macrophages. TUG-891 further decreased ROS production when compared to RANKL only cells. Antioxidant proteins, Nrf2, HO-1 and NQO1 were shown to be upregulated while the ROS inducing protein, Nox1, was downregulated by TUG-891. Gene silencing revealed that TUG-891 exerted its effects specifically through GPR120. This study reveals that GPR120 signalling may inhibit osteoclast formation and resorption through inhibition on ROS production.
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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.