ArticleInternational journal of molecular sciences2020
Cartilage Trauma Induces Necroptotic Chondrocyte Death and Expulsion of Cellular Contents.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Nucleic Acids as Emerging Regulators of Calcium Phosphate Biomineralization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Endocrine‑metabolic imbalance drives osteoarthritis: From whole‑joint pathobiology to precision therapy (Review).International journal of molecular medicine · 2026Review
- Analysis of cartilage creep-recovery of human osteoarthritic cartilage.European journal of medical research · 2026Article
- Focus on necroptosis: its role in the pathogenesis and therapeutic potential of osteoarthritis.Frontiers in immunology · 2026Review
- Significance of Necroptosis in Cartilage Degeneration.Biomolecules · 2024Review
- Osteoking promotes bone formation and bone defect repair through ZBP1-STAT1-PKR-MLKL-mediated necroptosis.Chinese medicine · 2024Article
- Chondrocyte Homeostasis and Differentiation: Transcriptional Control and Signaling in Healthy and Osteoarthritic Conditions.Life (Basel, Switzerland) · 2023Review
- RIP kinases and necroptosis in aging and aging-related diseases.Life medicine · 2022Review
- The role of necroptosis in disease and treatment.MedComm · 2021Review
- General Caspase Inhibition in Primary Chondrogenic Cultures Impacts Their Transcription Profile Including Osteoarthritis-Related Factors.Cartilage · 2021Article
- Therapeutic Potential of Bioactive Compounds in Honey for Treating Osteoarthritis.Frontiers in pharmacology · 2021Review
- RIP1 Perturbation Induces Chondrocyte Necroptosis and Promotes Osteoarthritis PathogenesisFrontiers in cell and developmental biology · 2021Article
- TRIM24-RIP3 axis perturbation accelerates osteoarthritis pathogenesis.Annals of the rheumatic diseases · 2020Article
- Extracellular Vesicles in Musculoskeletal Pathologies and Regeneration.Frontiers in bioengineering and biotechnology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptotic cell death is characterized by an activation of RIPK3 and MLKL that leads to plasma membrane permeabilization and the release of immunostimulatory cellular contents. High levels of chondrocyte death occur following intra-articular trauma, which frequently leads to post-traumatic osteoarthritis development. The aim of this study is to assess necroptosis levels in cartilage post-trauma and to examine whether chondrocyte necroptotic mechanisms may be investigated and modified in vitro. Fractured human and murine cartilage, analysed immunohistochemically for necroptosis marker expression, demonstrated significantly higher levels of RIPK3 and phospho-MLKL than uninjured controls. Primary murine chondrocytes stimulated in vitro with the TNFα and AKT-inhibitor alongside the pan-caspase inhibitor Z-VAD-fmk exhibited a significant loss of metabolic activity and viability, accompanied by an increase in MLKL phosphorylation, which was rescued by further treatment of chondrocytes with necrostatin-1. Transmission electron microscopy demonstrated morphological features of necroptosis in chondrocytes following TNFα and Z-VAD-fmk treatment. Release of dsDNA from necroptotic chondrocytes was found to be significantly increased compared to controls. This study demonstrates that cartilage trauma leads to a high prevalence of necroptotic chondrocyte death, which can be induced and inhibited in vitro, indicating that both necroptosis and its consequential release of immunostimulatory cellular contents are potential therapeutic targets in post-traumatic arthritis treatment.
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