ArticleCell death & disease2024
IL-17 promotes osteoclast-induced bone loss by regulating glutamine-dependent energy metabolism.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 39 citations in OpenAlex.
- Targeting the gut-bone axis in osteoporosis: probiotic interventions and other microbiota-based therapeutic strategies.Gut microbes · 2026Review
- Glycolysis in bone remodeling: from energy supply to signaling regulation.Molecular biology reports · 2026Review
- A microbiota-substrate-metabolite-target network suggests AKT1-associated links between gut microbiota-derived metabolites and osteoporosis.International microbiology : the official journal of the Spanish Society for Microbiology · 2026Article
- Impaired Bone Physiology in Rheumatoid Arthritis: Can the Wnt Pathway be the Connecting Link Between the Synovium and the Bone?Mediterranean journal of rheumatology · 2026Review
- Histone H3K18 lactylation: An exercise-induced epigenetic mechanism that inhibits osteoclast activity and protects against osteoporosis.Journal of orthopaedic translation · 2026Article
- Potential value of vitamin D as adjunctive therapy in osteoarticular tuberculosis: a comprehensive review.Infection · 2026Review
- Enhancer-directed gene delivery for digit regeneration based on conserved epidermal factors.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Spectrum and functions of ion channels and transporters in osteoclasts.Bone research · 2026Review
- The osteoclast intracellular environment fosters bacterial growth duringbioRxiv : the preprint server for biology · 2026Article
- Bone Marrow Immunometabolic Remodeling in Osteoporosis: From Systemic Risk Factors to Precision Intervention.International journal of general medicine · 2026Review
- The recent progression of extracellular vesicles application in osteoporosis.Frontiers in pharmacology · 2026Review
- Amino Acid Metabolic Enzymes in Gastric Cancer: Roles and Mechanisms in Tumorigenesis and Progression.Oncology research · 2026Review
- cGAS-STING pathway mediation in osteoclast function and bone fracture healing.Frontiers in immunology · 2026Article
- Roles of gut metabolites on bone mineralization and remodeling: impact of metabolic dysregulation on the gut-immune-bone axis.Frontiers in endocrinology · 2026Review
- Tri-Functional MgTA@MnOInternational journal of nanomedicine · 2026Article
- Combination of single-cell and bulk RNA-seq reveals changes in the immune landscape in osteomyelitis.Frontiers in immunology · 2026Article
- Secukinumab and Adalimumab on Bone Health in Psoriasis: A Longitudinal Cohort Study.Psoriasis (Auckland, N.Z.) · 2026Article
- Mitochondrial dysfunction in mesenchymal stem cells impairs osteogenesis in radiation-induced bone injury via CaCell death & disease · 2025Article
- Enhancer-directed gene delivery for digit regeneration based on conserved epidermal factors.bioRxiv : the preprint server for biology · 2025Article
- Inhibition of integrin α3 suppresses gastric cancer progression via STAT3-mediated regulation of SLC1A5-dependent glutamine uptake.Journal of gastroenterology · 2025Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Osteoclasts consume an amount of adenosine triphosphate (ATP) to perform their bone resorption function in the development of osteoporosis. However, the mechanism underlying osteoclast energy metabolism has not been fully elucidated. In addition to glucose, glutamine (Glu) is another major energy carrier to produce ATP. However, the role of Glu metabolism in osteoclasts and the related molecular mechanisms has been poorly elucidated. Here we show that Glu is required for osteoclast differentiation and function, and that Glu deprivation or pharmacological inhibition of Glu transporter ASCT2 by V9302 suppresses osteoclast differentiation and their bone resorptive function. In vivo treatment with V9302 improved OVX-induced bone loss. Mechanistically, RNA-seq combined with in vitro and in vivo experiments suggested that Glu mediates the role of IL-17 in promoting osteoclast differentiation and in regulating energy metabolism. In vivo IL-17 treatment exacerbated OVX-induced bone loss, and this effect requires the participation of Glu or its downstream metabolite α-KG. Taken together, this study revealed a previously unappreciated regulation of IL-17 on energy metabolism, and this regulation is Glu-dependent. Targeting the IL-17-Glu-energy metabolism axis may be a potential therapeutic strategy for the treatment of osteoporosis and other IL-17 related 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.