ArticleFrontiers in bioengineering and biotechnology2025
Necrostatin-1 alleviates temporomandibular joint osteoarthritis and inhibits chondrocyte senescence and necroptosis possibly via p53/ MAPK downregulation.
Article in Frontiers in bioengineering and biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Mitochondrial quality control modulating chondrocyte behavior and fate in knee osteoarthritis: mechanistic insights and therapeutic prospects.Frontiers in immunology · 2026Review
- Tat-HSPE1 suppresses clear cell renal cell carcinoma growth through lysosome-dependent cell death.Frontiers in pharmacology · 2026Article
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Abstract
Temporomandibular joint osteoarthritis (TMJ-OA) is a prevalent oral and maxillofacial disorder characterized by a complex etiology and pathogenesis. Targeting and eliminating senescent chondrocytes is emerging as a promising therapeutic strategy for TMJ-OA. Necrostatin-1 (NEC1), a receptor-interacting protein kinase 1 (RIPK1)-targeted necroptosis inhibitor, has shown potential therapeutic effects in various skeletal disorders. However, the therapeutic implications of NEC1 in TMJ-OA, particularly regarding its effect on chondrocyte senescence, remain unclear. In this study, models of TMJ-OA were established by utilizing monosodium iodoacetate (MIA) to induce TMJ-OA in rats. NEC1 was administered via intra-articular injection. Treatment with NEC1 significantly alleviated the progression of TMJ-OA in rats, reduced pain, and restored cartilage integrity.
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