ArticleArchives of toxicology2025
Targeting MLKL ameliorates T-2 toxin-induced cartilage damage by inhibiting chondrocyte death and matrix degradation in mice.
Article in Archives of toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
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Who cites it
2 citing papers in PubMed.
- GPx6 downregulation drives ferroptosis in Kashin-Beck disease chondrocytes via the SLC7A11/GPx4 axis.Apoptosis : an international journal on programmed cell death · 2026Article
- Focus on necroptosis: its role in the pathogenesis and therapeutic potential of osteoarthritis.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
T-2 toxin is the most toxic mycotoxin found in contaminated food and animal feed that threatens health. Exposure to T-2 toxin causes cartilage damage and leads to joint disorders, but the mechanisms underlying T-2 toxin-induced cartilage damage remain unclear. The results showed that T-2 toxin-induced chondrocyte death in articular cartilage from rats fed T-2 toxin (200 ng/g b.w./day) caused a significant increase in phosphorylated receptor-interacting protein 3 (p-RIPK3) and phosphorylated mixed lineage kinase-like protein (p-MLKL). In vitro studies showed that T-2 toxin (48 ng/mL) reduced the viability of C-28/I2 chondrocytes, increased cell apoptosis, and significantly upregulated the expression of p-MLKL. The results suggest that chondrocyte necroptosis is involved in T-2 toxin-induced cartilage damage. Furthermore, necrostatin-1 (Nec-1), a necroptosis inhibitor, significantly attenuated T-2 toxin-induced cell death and the increase of p-MLKL. Further studies showed that mlkl
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Registered trials
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