ArticleMolecular therapy : the journal of the American Society of Gene Therapy2023
Inhibition of C5AR1 impairs osteoclast mobilization and prevents bone loss.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- Trial
- Gestational Protein Restriction Promotes Osteoporotic Phenotype During Aging.Calcified tissue international · 2026Article
- Targeting innate immunity to modulate bone metabolism: a novel strategy for osteoporosis treatment.Frontiers in aging · 2026Review
- Current Progress of Hederagenin and Its Derivatives for Disease Therapy (2017-Present).Molecules (Basel, Switzerland) · 2025Review
- AMY-101 as complement C3 inhibitor for periodontitis therapy: mechanisms, efficacy, and clinical translation.Frontiers in immunology · 2025Review
- IL7-IL7R Interaction Mediates Fibroblast-Driven Macrophage-to-Osteoclast Differentiation in Periodontitis.Journal of inflammation research · 2025Article
- Bone-protective effects of deer-hide gelatin in cyclophosphamide-induced osteoporosis rats.Frontiers in pharmacology · 2025Article
- Article
- Ageing-related bone and immunity changes: insights into the complex interplay between the skeleton and the immune system.Bone research · 2024Review
- Osteoclasts and osteoarthritis: Novel intervention targets and therapeutic potentials during aging.Aging cell · 2024Review
- Single-cell Atlas reveals core function of CPVL/MSR1 expressing macrophages in the prognosis of triple-negative breast cancer.Frontiers in immunology · 2024Article
- Atsttrin regulates osteoblastogenesis and osteoclastogenesis through the TNFR pathway.Communications biology · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related and chemotherapy-induced bone loss depends on cellular senescence and the cell secretory phenotype. However, the factors secreted in the senescent microenvironment that contribute to bone loss remain elusive. Here, we report a central role for the inflammatory alternative complement system in skeletal bone loss. Through transcriptomic analysis of bone samples, we identified complement factor D, a rate-limiting factor of the alternative pathway of complement, which is among the most responsive factors to chemotherapy or estrogen deficiency. We show that osteoblasts and osteocytes are major inducers of complement activation, while monocytes and osteoclasts are their primary targets. Genetic deletion of C5ar1, the receptor of the anaphylatoxin C5a, or treatment with a C5AR1 inhibitor reduced monocyte chemotaxis and osteoclast differentiation. Moreover, genetic deficiency or inhibition of C5AR1 partially prevented bone loss and osteoclastogenesis upon chemotherapy or ovariectomy. Altogether, these lines of evidence support the idea that inhibition of alternative complement pathways may have some therapeutic benefit in osteopenic disorders.
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