ArticleArthritis research & therapy2025
CXCL7 enhances RANKL-induced osteoclastogenesis via the activation of ERK/NFATc1 signaling pathway in inflammatory arthritis.
Article in Arthritis research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- PPBP orchestrates autophagy-apoptosis imbalance to drive cartilage degeneration in osteoarthritis.Biology direct · 2026Article
- Alpha2EQ downregulates proinflammatory cytokine and chemokine gene expression in cultured synovial fibroblasts.American journal of veterinary research · 2026Article
- IL-34-mediated fibroblast-like synoviocyte-macrophage crosstalk drives bone erosion in rheumatoid arthritis through RANKL-dependent osteoclastogenesis.Frontiers in immunology · 2026Article
- Eucommia ulmoides extract and soy isoflavones attenuate postmenopausal osteoporosis by modulating bone-specific transcription factors and inflammatory signaling pathways.Frontiers in pharmacology · 2026Article
- Apoptotic vesicles rectify senile bone-fat imbalance by activating Thy1-ERK-TAZ axis.Journal of nanobiotechnology · 2025Article
- Single-cell RNA sequencing reveals NFATc1-mediated regulatory mechanisms of vascular smooth muscle cell osteogenic transformation in the osteosarcoma microenvironment.Discover oncology · 2025Article
- CXCL7 promotes bone erosion in RA.Nature reviews. Rheumatology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundRheumatoid arthritis (RA) with anti-citrullinated protein/peptide antibodies (ACPA + RA) demonstrates more significant radiographic damage compared to ACPA-negative RA (ACPA- RA). Chemokine-activated signaling pathways contribute to the regulation of the bone formation and resorption. The potential role of C-X-C motif chemokine ligand 7 (CXCL7) in bone erosion and its viability as a therapeutic target for RA merit further investigation.
methodsPlasma CXCL7 concentration was quantified using enzyme-linked immunosorbent assay (ELISA). The effect of CXCL7 on receptor activator of NF-κB ligand (RANKL)-induced osteoclastogeneis was assessed through tartrate-resistant acid phosphates (TRAP) staining and F-actin ring immunofluorescence. Western blotting analysis was used to identify the signaling pathways activated by CXCL7. To investigate the potential therapeutic effect by targeting Cxcl7, Cxcl7 neutralizing antibodies were administrated intraperitoneally to mice with collagen-induced arthritis (CIA). Histopathology and micro-computed tomography (micro-CT) scanning were utilized to assess joint inflammation and bone destruction in CIA mice.
resultsThe plasma CXCL7 concentration was significantly higher in ACPA + RA compared with ACPA- RA and healthy controls. The level of CXCL7 was positively correlated with disease activity and bone erosion in RA patients. It was discovered that CXCL7 promoted RANKL-induced osteoclastogenesis in CD14 + monocytes derived from RA patients. Mechanistically, the addition of Cxcl7 significantly enhanced RANKL-induced phosphorylation of ERK1/2 and NFATc1 expresssion. Cxcl7 neutralizing antibody alleviated arthritis severity in CIA by reducing the inflammatory response, osteoclasts numbers, and bone destruction in CIA mice joints.
conclusionCXCL7 contributes to the bone erosion in RA by enhancing RANKL-induced osteoclastogenesis via the activation of ERK/NFATc1 signaling pathways. CXCL7 could potentially be targeted for therapeutic interventions in RA.
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.