ArticleNature communications2021
Osteoclast fusion and bone loss are restricted by interferon inducible guanylate binding proteins.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
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
59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.
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- The Effects ofNutrients · 2023Pooled it
- Apoptosis-resistant megakaryocytes produce large and hyperreactive platelets in response to radiation injury.Military Medical Research · 2023Trial
- Cytokine Regulation of the Bone Pre- and Metastatic Niches: Implications for Breast Cancer Dormancy.Cells · 2026Review
- IRF1 regulates apoptosis and osteogenic differentiation of bone marrow mesenchymal stem cells and ameliorates osteoporosis by activating the PI3K/AKT signaling pathway.Journal of advanced research · 2026Article
- Transcriptome Analysis of Differentially Expressed Genes and Molecular Pathways Involved During Osteoclast Differentiation.Molecular biotechnology · 2026Article
- Engineering Osteoimmune Responses with Functionalized Orthopedic Implants for Post-Operative Osteosarcoma Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Porphyromonas gingivalis-Derived Virulence Lipids Accelerate Osteoclastogenesis Independently of High Mobility Group Box Protein-1 Canonical Signaling.Molecular oral microbiology · 2026Article
- Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026Review
- Osteoblast-derived osteomodulin restrains osteoclastogenesis via ITGB8/RRM2-mediated reduction of mitochondrial respiration and mitochondrial ATP production.Experimental & molecular medicine · 2026Article
- Research on fall prediction in elderly patients with chronic diseases based on explainable machine learning: an aging perspective.BMC geriatrics · 2026Article
- Aebp1 loss in osteoprogenitors leads to skeletal defects resembling Ehlers-Danlos Syndrome by diminishing Wnt/β-catenin signaling.JCI insight · 2026Article
- Role of Cytokines in Bone Diseases and Their Therapeutic Application.ImmunoTargets and therapy · 2026Review
- Cynarin as a potent anti‑osteolytic agent: Targeting MAPK and Nrf2‑Keap1 pathways for osteoclast inhibition and bone protection.International journal of molecular medicine · 2025Article
- Dual regulation of phaseol on osteoclast formation and osteoblast differentiation by targeting TAK1 kinase for osteoporosis treatment.Journal of advanced research · 2025Article
- Guanylate-binding protein 5: a promising biomarker and therapeutic target.Infection and immunity · 2025Review
- Article
- Direct microglia replacement reveals pathologic and therapeutic contributions of brain macrophages to a monogenic neurological disease.Immunity · 2025Article
- Role of guanylate-binding protein 5 in inflammatory diseases, immune diseases, cancers, and its potential therapeutic implications.Inflammopharmacology · 2025Review
- Spatiotemporal application of small molecules in fracture healing.Biomaterials translational · 2025Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Chronic inflammation during many diseases is associated with bone loss. While interferons (IFNs) are often inhibitory to osteoclast formation, the complex role that IFN and interferon-stimulated genes (ISGs) play in osteoimmunology during inflammatory diseases is still poorly understood. We show that mice deficient in IFN signaling components including IFN alpha and beta receptor 1 (IFNAR1), interferon regulatory factor 1 (IRF1), IRF9, and STAT1 each have reduced bone density and increased osteoclastogenesis compared to wild type mice. The IFN-inducible guanylate-binding proteins (GBPs) on mouse chromosome 3 (GBP1, GBP2, GBP3, GBP5, GBP7) are required to negatively regulate age-associated bone loss and osteoclastogenesis. Mechanistically, GBP2 and GBP5 both negatively regulate in vitro osteoclast differentiation, and loss of GBP5, but not GBP2, results in greater age-associated bone loss in mice. Moreover, mice deficient in GBP5 or chromosome 3 GBPs have greater LPS-mediated inflammatory bone loss compared to wild type mice. Overall, we find that GBP5 contributes to restricting age-associated and inflammation-induced bone loss by negatively 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 OpenQuestion graph.