ArticleNature medicine2009
Estrogen-dependent and C-C chemokine receptor-2-dependent pathways determine osteoclast behavior in osteoporosis.
Article in Nature medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.
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Who cites it
108 citing papers in PubMed, 1 synthesis or guideline pooled it, 209 citations in OpenAlex.
- Meta-analysis of gene-based genome-wide association studies of bone mineral density in Chinese and European subjects.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2012Pooled it
- Trial
- Gestational Protein Restriction Promotes Osteoporotic Phenotype During Aging.Calcified tissue international · 2026Article
- Piezo1 activation suppresses bone marrow adipogenesis to prevent osteoporosis by inhibiting a mechanoinflammatory autocrine loop.Signal transduction and targeted therapy · 2025Article
- The circadian regulator PER1 inhibits osteoclastogenesis by activating inflammatory genes.bioRxiv : the preprint server for biology · 2025Article
- Targeting miR-337 mitigates disuse-induced bone loss.Cell discovery · 2025Article
- Comparative Evaluation of Compression Testing Methods for Murine Lumbar Vertebral Bodies: Identifying Most Reliable and Reproducible Techniques for Assessing Compressive Strength.Bioengineering (Basel, Switzerland) · 2025Article
- Disulfiram ameliorates bone loss in ovariectomized mice by suppressing osteoclastogenesis.Journal of bone and mineral metabolism · 2025Article
- CCL2/CCR2 Signalling in Mesenchymal Stem/Progenitor Cell Recruitment and Fracture Healing in Mice.Journal of cellular and molecular medicine · 2024Article
- Cell fusion dynamics: mechanisms of multinucleation in osteoclasts and macrophages.Inflammation and regeneration · 2024Review
- Cellular signatures in human blood track bone mineral density in postmenopausal women.JCI insight · 2024Article
- Lymphotoxin-β promotes breast cancer bone metastasis colonization and osteolytic outgrowth.Nature cell biology · 2024Article
- Hdac3 deficiency limits periosteal reaction associated with Western diet feeding in female mice.Journal of cellular and molecular medicine · 2024Article
- SOXC are critical regulators of adult bone mass.Nature communications · 2024Article
- Neutrophils in Inflammatory Bone Diseases.Current osteoporosis reports · 2024Review
- Osteoclasts at Bone Remodeling: Order from Order.Results and problems in cell differentiation · 2024Review
- An exploration of the causal relationship between 731 immunophenotypes and osteoporosis: a bidirectional Mendelian randomized study.Frontiers in endocrinology · 2024Article
- Screening diagnostic markers of osteoporosis based on ferroptosis of osteoblast and osteoclast.Aging · 2023Article
- Novel one-pot strategy for fabrication of a pH-Responsive bone-targeted drug self-frame delivery system for treatment of osteoporosis.Materials today. Bio · 2023Article
- Identification of 12 hub genes associated to the pathogenesis of osteoporosis based on microarray and single-cell RNA sequencing data.Functional & integrative genomics · 2023Article
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the mechanisms of osteoclastogenesis is crucial for developing new drugs to treat diseases associated with bone loss, such as osteoporosis. Here we report that the C-C chemokine receptor-2 (CCR2) is crucially involved in balancing bone mass. CCR2-knockout mice have high bone mass owing to a decrease in number, size and function of osteoclasts. In normal mice, activation of CCR2 in osteoclast progenitor cells results in both nuclear factor-kappaB (NF-kappaB) and extracellular signal-related kinase 1 and 2 (ERK1/2) signaling but not that of p38 mitogen-activated protein kinase or c-Jun N-terminal kinase. The induction of NF-kappaB and ERK1/2 signaling in turn leads to increased surface expression of receptor activator of NF-kappaB (RANK, encoded by Tnfrsf11a), making the progenitor cells more susceptible to RANK ligand-induced osteoclastogenesis. In ovariectomized mice, a model of postmenopausal osteoporosis, CCR2 is upregulated on wild-type preosteoclasts, thus increasing the surface expression of RANK on these cells and their osteoclastogenic potential, whereas CCR2-knockout mice are resistant to ovariectomy-induced bone loss. These data reveal a previously undescribed pathway by which RANK, osteoclasts and bone homeostasis are regulated in health and disease.
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