ArticleArthritis research & therapy2021
Gasdermin D deficiency attenuates arthritis induced by traumatic injury but not autoantibody-assembled immune complexes.
Article in Arthritis research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Osteocyte-specific gasdermin D deletion accelerates osteoarthritis via promoting subchondral inflammation and remodeling.Bone research · 2026Article
- Patellar luxation causes abnormal mechanical loading and joint destruction in the femoral-tibial joint.Bone & joint research · 2026Article
- Single-Cell Genetic Mapping of Gasdermin Expression Across Immune-Mediated Inflammatory Diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Focus on the NLRP3 inflammasome: its role in the pathogenesis and therapeutic potential of inflammation-driven osteoarthritis.Frontiers in immunology · 2026Review
- Activation of the noncanonical inflammasome-GSDMD pathway triggers pyroptosis in bone marrow and promotes periosteal bone formation.bioRxiv : the preprint server for biology · 2025Article
- Programmed Cell Death of Chondrocytes, Synovial Cells, Osteoclasts, and Subchondral Bone Cells in Osteoarthritis.Journal of inflammation research · 2025Review
- Mechanisms of chondrocyte cell death in osteoarthritis: implications for disease progression and treatment.Journal of orthopaedic surgery and research · 2024Review
- Pyroptosis in Osteoarthritis: Molecular Mechanisms and Therapeutic Implications.Journal of inflammation research · 2024Review
- The Role of Gasdermin-D-Mediated Pyroptosis in Organ Injury and Its Therapeutic Implications.Organogenesis · 2023Review
- Pyroptosis in bone loss.Apoptosis : an international journal on programmed cell death · 2023Review
- Protein phosphatase PPM1A inhibition attenuates osteoarthritis via regulating TGF-β/Smad2 signaling in chondrocytes.JCI insight · 2023Article
- Targeting inflammasome-dependent mechanisms as an emerging pharmacological approach for osteoarthritis therapy.iScience · 2022Review
- The regulatory role and therapeutic application of pyroptosis in musculoskeletal diseases.Cell death discovery · 2022Review
- No longer married to inflammasome signaling: the diverse interacting pathways leading to pyroptotic cell death.The Biochemical journal · 2022Review
- How Pyroptosis Contributes to Inflammation and Fibroblast-Macrophage Cross-Talk in Rheumatoid Arthritis.Cells · 2022Review
- Pyroptosis: A Novel Intervention Target in the Progression of Osteoarthritis.Journal of inflammation research · 2022Review
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundGasdermin D (GSDMD) is cleaved by several proteases including by caspase-1, a component of intracellular protein complexes called inflammasomes. Caspase-1 also converts pro-interleukin-1β (pro-IL-1β) and pro-IL-18 into bioactive IL-1β and IL-18, respectively. GSDMD amino-terminal fragments form plasma membrane pores, which mediate the secretion of IL-1β and IL-18 and cause the inflammatory form of cell death pyroptosis. Here, we tested the hypothesis that GSDMD contributes to joint degeneration in the K/BxN serum transfer-induced arthritis (STIA) model in which autoantibodies against glucose-6-phosphate isomerase promote the formation of pathogenic immune complexes on the surface of myeloid cells, which highly express the inflammasomes. The unexpected outcomes with the STIA model prompted us to determine the role of GSDMD in the post-traumatic osteoarthritis (PTOA) model caused by meniscus ligamentous injury (MLI) based on the hypothesis that this pore-forming protein is activated by signals released from damaged joint tissues.
methodsGsdmd
resultsGSDMD levels were higher in serum-inoculated paws compared to PBS-injected paws. Unexpectedly, ablation of GSDMD failed to reduce joint swelling and osteolysis, suggesting that GSDMD was dispensable for the pathogenesis of STIA. GSDMD levels were also higher in MLI compared to sham-operated joints. Importantly, ablation of GSDMD attenuated MLI-associated cartilage degradation (p = 0.0097), synovitis (p = 0.014), subchondral bone sclerosis (p = 0.0006), and subchondral bone plate thickness (p = 0.0174) based on histopathological and μCT analyses.
conclusionGSDMD plays a key role in the pathogenesis of PTOA, but not STIA, suggesting that its actions in experimental arthropathy are tissue context-specific.
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