ArticleCommunications biology2022
gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 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
18 citing papers in PubMed, 23 citations in OpenAlex.
- GP130 Regulates Macrophage Polarization and Functional Recovery after Spinal Cord Injury in Rats: A Single-Cell RNA Sequencing Study.Inflammation · 2026Article
- Circulating Exosomal MicroRNA Profiles Associated with Heavy Metal Exposure and Short Stature in Children.International journal of molecular sciences · 2026Article
- Stress-induced IL-6 regulation in pediatric bone growth disorders: current insights and therapeutic strategies.Frontiers in endocrinology · 2026Review
- Beyond resorption-driven coupling: a multi-layered framework for osteoclast-osteoblast communication and its therapeutic consequences.Frontiers in endocrinology · 2026Review
- Reg3β promotes chondrocyte proliferation and ECM metabolism during acetabular roof remodeling in a rat model of DDH‑induced residual dysplasia.Molecular medicine reports · 2025Article
- Therapeutic potential of peptidomimetics of suppressors of cytokine signaling (SOCS) proteins in rheumatic disorders.Frontiers in medicine · 2025Article
- Article
- Application of kartogenin for the treatment of cartilage defects: current practice and future directions.RSC advances · 2024Review
- IL-6R (trans-signaling) is a key regulator of reverse cholesterol transport in lipid-laden macrophages.Clinical immunology (Orlando, Fla.) · 2024Article
- HIF-1α and MIF enhance neutrophil-driven type 3 immunity and chondrogenesis in a murine spondyloarthritis model.Cellular & molecular immunology · 2024Article
- MiR-653-5p drives osteoarthritis pathogenesis by modulating chondrocyte senescence.Arthritis research & therapy · 2024Article
- Review
- Contribution of Signal Transducer and Activator of Transcription 3 (STAT3) to Bone Development and Repair.International journal of molecular sciences · 2023Article
- Inhibition of a signaling modality within the gp130 receptor enhances tissue regeneration and mitigates osteoarthritis.Science translational medicine · 2023Article
- Article
- Differences in Synovial Cytokine Profile Associated with Long-Term Clinical Outcomes in Patients with Knee Osteoarthritis Undergoing Corrective Osteotomy with Platelet-Rich Plasma or Stromal Vascular Fraction Post-Treatments.International journal of molecular sciences · 2022Article
- Article
- Stat3 Signaling Pathway: A Future Therapeutic Target for Bone-Related Diseases.Frontiers in pharmacology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
Abstract
Growth of long bones and vertebrae is maintained postnatally by a long-lasting pool of progenitor cells. Little is known about the molecular mechanisms that regulate the output and maintenance of the cells that give rise to mature cartilage. Here we demonstrate that postnatal chondrocyte-specific deletion of a transcription factor Stat3 results in severely reduced proliferation coupled with increased hypertrophy, growth plate fusion, stunting and signs of progressive dysfunction of the articular cartilage. This effect is dimorphic, with females more strongly affected than males. Chondrocyte-specific deletion of the IL-6 family cytokine receptor gp130, which activates Stat3, phenocopied Stat3-deletion; deletion of Lifr, one of many co-receptors that signals through gp130, resulted in a milder phenotype. These data define a molecular circuit that regulates chondrogenic cell maintenance and output and reveals a pivotal positive function of IL-6 family cytokines in the skeletal system with direct implications for skeletal development and regeneration.
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.