ArticleBlood2010
Efficient osteoclast differentiation requires local complement activation.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 71 citations in OpenAlex.
- Trial
- Targeting innate immunity to modulate bone metabolism: a novel strategy for osteoporosis treatment.Frontiers in aging · 2026Review
- Mixed effects of complement in a chronic murine model of inflammatory erosive arthritis and pulmonary vascular disease.PloS one · 2026Article
- Knockdown of C3aR alleviates age-related bone loss via activation of YAP1/β-catenin signaling.The Journal of biological chemistry · 2025Article
- Complement C3a promotes the formation of osteoclasts by inhibiting Sirt1 to activate the PI3K/PDK1/SGK3 pathway in patients with multiple myeloma.Journal of translational medicine · 2025Article
- Single-cell multi-omics identify novel regulators required for osteoclastogenesis during aging.iScience · 2024Article
- Article
- Label-free quantitative proteomics in serum reveals candidate biomarkers associated with low bone mineral density in Mexican postmenopausal women.GeroScience · 2024Article
- The heart-bone connection: relationships between myocardial infarction and osteoporotic fracture.American journal of physiology. Heart and circulatory physiology · 2024Review
- The association of an elevated Th/Ts ratio and lupus anticoagulant with symptomatic osteonecrosis in systemic lupus erythematosus patients.Frontiers in immunology · 2024Article
- Complement Receptor C3aR1 Contributes to Paclitaxel-Induced Peripheral Neuropathic Pain in Mice and Rats.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Inhibition of C5AR1 impairs osteoclast mobilization and prevents bone loss.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- C3a-C3aR signaling is a novel modulator of skeletal homeostasis.Bone reports · 2023Article
- New insight of complement system in the process of vascular calcification.Journal of cellular and molecular medicine · 2023Review
- Exercise Promotes Bone Marrow Microenvironment by Inhibiting Adipsin in Diet-Induced Male Obese Mice.Nutrients · 2022Article
- Topography-mediated immunomodulation in osseointegration; Ally or Enemy.Biomaterials · 2022Review
- Complement receptor C5aR1 on osteoblasts regulates osteoclastogenesis in experimental postmenopausal osteoporosis.Frontiers in endocrinology · 2022Article
- Effects of an Environmentally Relevant Mixture of Organophosphate Esters Derived From House Dust on Endochondral Ossification in Murine Limb Bud Cultures.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Bone marrow adipogenic lineage precursors promote osteoclastogenesis in bone remodeling and pathologic bone loss.The Journal of clinical investigation · 2021Article
- Activated Hepatic Stellate Cells (HSCs) Exert Immunosuppressive Effects in Hepatocellular Carcinoma by Producing Complement C3.OncoTargets and therapy · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies using blocking antibodies suggested that bone marrow (BM)-derived C3 is required for efficient osteoclast (OC) differentiation, and that C3 receptors are involved in this process. However, the detailed underlying mechanism and the possible involvement of other complement receptors remain unclear. In this report, we found that C3(-/-) BM cells exhibited lower RANKL/OPG expression ratios, produced smaller amounts of macrophage colony-stimulating factor and interleukin-6 (IL-6), and generated significantly fewer OCs than wild-type (WT) BM cells. During differentiation, in addition to C3, WT BM cells locally produced all other complement components required to activate C3 and to generate C3a/C5a through the alter-native pathway, which is required for efficient OC differentiation. Abrogating C3aR/C5aR activity either genetically or pharmaceutically suppressed OC generation, while stimulating WT or C3(-/-) BM cells with exogenous C3a and/or C5a augmented OC differentiation. Furthermore, supplementation with IL-6 rescued OC generation from C3(-/-) BM cells, and neutralizing antibodies to IL-6 abolished the stimulatory effects of C3a/C5a on OC differentiation. These data indicate that during OC differentiation, BM cells locally produce components, which are activated through the alternative pathway to regulate OC differentiation. In addition to C3 receptors, C3aR/C5aR also regulate OC differentiation, at least in part, by modulating local IL-6 production.
Indexed as
Identifiers
What OpenQuestion holds
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.