ArticleArthritis research & therapy2023
STING mediates experimental osteoarthritis and mechanical allodynia in mouse.
Article in Arthritis research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Aerobic Exercise Mitigates Experimental Knee Osteoarthritis via Inhibition of cGAS-STING Signaling.Microbiology and immunology · 2026Article
- New Adjuvant Therapies for Obesity-Related Disorders Associated with Meta-Neuroinflammation.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Automated Objective Scoring of Osteoarthritis Severity in Mouse Medial Tibial Cartilage Using Deep Learning.Cartilage · 2026Article
- Extracellular vesicles from IPFP-MSCs trigger osteoarthritis by transferring mtDNA.Bioactive materials · 2026Article
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- Revisiting osteoarthritis pathogenesis through the lens of cGAS-STING: Mitochondrial damage, pyroptosis, and inflammatory cascades.Journal of orthopaedic translation · 2026Review
- How Selective are Nanomaterials to Treat Osteoarthritis.International journal of nanomedicine · 2026Review
- NF-κB signaling in osteoarthritis: integrating mechanical stress, innate immunity, and cartilage degeneration.Frontiers in immunology · 2026Review
- Dysfunctional autophagy triggers STING1 activation to exacerbate cartilage degeneration in obesity-associated osteoarthritis.Autophagy · 2025Article
- A Review of Rodent Behavior, Mobility, and Pain Modifications in Response to Destabilization of the Medial Meniscus Injury.Biomedicines · 2025Review
- TRPM2-mediated feed-forward loop promotes chondrocyte damage in osteoarthritis via calcium-cGAS-STING-NF-κB pathway.Journal of advanced research · 2025Article
- Article
- Recent advances in targeting the cGAS-STING pathway for immunotherapy in orthopedic diseases.Frontiers in immunology · 2025Review
- Targeting Caspase-1 in osteoarthritis: multi-omics insights into the effects of VX-765 on human chondrocyte function and phenotype.Frontiers in immunology · 2025Article
- Acacetin targets STING to alleviate the destabilization of the medial meniscus-induced osteoarthritis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- cGAS-STING pathway in pathogenesis and treatment of osteoarthritis and rheumatoid arthritis.Frontiers in immunology · 2024Review
- Prokineticin 2 is a catabolic regulator of osteoarthritic cartilage destruction in mouse.Arthritis research & therapy · 2023Article
- STING signaling in inflammaging: a new target against musculoskeletal diseases.Frontiers in immunology · 2023Review
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4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study was performed to develop therapeutic targets of osteoarthritis (OA) that can be targeted to alleviate OA development (i.e., cartilage destruction) and relieve the OA-associated joint pain.
methodsThe candidate molecule, STING (stimulator of interferon genes, encoded by Sting1), was identified by microarray analysis of OA-like mouse chondrocytes. Experimental OA in mice was induced by destabilization of the medial meniscus (DMM). STING functions in OA and hindpaw mechanical allodynia were evaluated by gain-of-function (intra-articular injection of a STING agonist) and loss-of-function (Sting1-/- mice) approaches.
resultsDNA damage was observed in OA-like chondrocytes. Cytosolic DNA sensors, STING and its upstream molecule, cGAS (cyclic GMP-AMP synthase), were upregulated in OA chondrocytes and cartilage of mouse and human. Genetic ablation of STING in mice (Sting1-/-) alleviated OA manifestations (cartilage destruction and subchondral bone sclerosis) and hindpaw mechanical allodynia. In contrast, stimulation of STING signaling in joint tissues by intra-articular injection of cGAMP exacerbated OA manifestations and mechanical sensitization. Mechanistic studies on the regulation of hindpaw mechanical allodynia revealed that STING regulates the expression of peripheral sensitization molecules in the synovium and meniscus of mouse knee joints.
conclusionOur results indicated that STING, which senses damaged cytosolic DNA and accordingly activates the innate immune response, regulates OA pathogenesis and hindpaw mechanical allodynia. Therefore, inhibition of STING could be a therapeutic approach to inhibit OA cartilage destruction and relieve the associated mechanical sensitization in model mice.
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