ReviewExperimental & molecular medicine2020
The JAK1/STAT3/SOCS3 axis in bone development, physiology, and pathology.
Review in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 89 citations in OpenAlex.
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- Dexmedetomidine alleviates acute lung injury in humans by modulating the JAK1-STAT3 axis.Experimental and therapeutic medicine · 2026Article
- Characterizing the effects of anti-PD1 immunotherapy on ataxia in a vestibular schwannoma mouse model.Journal of neuro-oncology · 2026Article
- Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026Review
- JAK-STAT signaling: molecular mechanism and targeted treatment in dento-maxillofacial abnormalities.International journal of oral science · 2026Review
- Glutamine alleviates Staphylococcus aureus-induced mastitis by modulating macrophage polarisation.PLoS pathogens · 2026Article
- Small-molecule therapies for pediatric inflammatory bowel disease: toward precision medicine.World journal of pediatrics : WJP · 2026Review
- Single-cell landscape of lymphoid and myeloid heterogeneity across type-stratified craniofacial lesions in polyostotic fibrous dysplasia.Frontiers in immunology · 2026Article
- Identification and validation of ferroptosis-related key hub genes linking hypoxia and osteoporosis.BMC musculoskeletal disorders · 2025Article
- Effect of membrane vesicles produced under different pH conditions on the ability ofJournal of bacteriology · 2025Article
- Genomic diversity and selection signatures in Asian Zebu Cattle: insights into adaptation and genetic erosion.Scientific reports · 2025Article
- IL6ST participates in the development of adolescent idiopathic scoliosis by regulating bone marrow mesenchymal stem cells.Communications biology · 2025Article
- Reduced somatosensory innervation alters the skeletal transcriptome at a single cell level in a mouse model of type 2 diabetes.Bone research · 2025Article
- Lacc1-engineered extracellular vesicles reprogram mitochondrial metabolism to alleviate inflammation and cartilage degeneration in TMJ osteoarthritis.Journal of nanobiotechnology · 2025Article
- Fracture-Induced Immunological Cascades Trigger Rapid Systemic Bone Loss via Osteocyte-Regulated Osteoclastogenesis.ImmunoTargets and therapy · 2025Article
- Exosome-Loaded Bioscaffolds for Spinal Cord Injuries: A Review.Stem cells international · 2025Review
- PF4 Silencing Promotes Trophoblast Cell Proliferation, Migration, Invasion and EMT by Regulating SOCS3/STAT3 Signaling Pathway.Endocrine, metabolic & immune disorders drug targets · 2024Article
- BMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarization.Molecular medicine (Cambridge, Mass.) · 2024Article
- Hemophagocytic lymphohistiocytosis: current treatment advances, emerging targeted therapy and underlying mechanisms.Journal of hematology & oncology · 2024Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Bone growth and the maintenance of bone structure are controlled by multiple endocrine and paracrine factors, including cytokines expressed locally within the bone microenvironment and those that are elevated, both locally and systemically, under inflammatory conditions. This review focuses on those bone-active cytokines that initiate JAK-STAT signaling, and outlines the discoveries made from studying skeletal defects caused by induced or spontaneous modifications in this pathway. Specifically, this review describes defects in JAK1, STAT3, and SOCS3 signaling in mouse models and in humans, including mutations designed to modify these pathways downstream of the gp130 coreceptor. It is shown that osteoclast formation is generally stimulated indirectly by these pathways through JAK1 and STAT3 actions in inflammatory and other accessory cells, including osteoblasts. In addition, in bone remodeling, osteoblast differentiation is increased secondary to stimulated osteoclast formation through an IL-6-dependent pathway. In growth plate chondrocytes, STAT3 signaling promotes the normal differentiation process that leads to bone lengthening. Within the osteoblast lineage, STAT3 signaling promotes bone formation in normal physiology and in response to mechanical loading through direct signaling in osteocytes. This activity, particularly that of the IL-6/gp130 family of cytokines, must be suppressed by SOCS3 for the normal formation of cortical bone.
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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 Socratic graph.