ArticleBiomolecules & biomedicine2025
Epigenetic mechanisms of Nsd1-mediated histone methylation modifications in chondrocyte ferroptosis in knee osteoarthritis.
Article in Biomolecules & biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Review
- Histone modifications: Unveiling the epigenetic enigma of degenerative skeletal diseases.Journal of orthopaedic translation · 2025Review
- Nuclear binding SET domain 1 alleviates cartilage ferroptosis in knee osteoarthritis by upregulating the krüppel-like factor 9/autophagy-related 14 pathway via H3K36me2 modification.Journal of cell communication and signaling · 2025Article
- Ferroptosis and bone health: bridging the gap between mechanisms and therapy.Frontiers in immunology · 2025Review
- The "gut microbiota-ferroptosis axis": a hypothesis for osteoarthritis pathogenesis and therapeutic implications.Frontiers in microbiology · 2025Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Knee osteoarthritis (KOA) is a degenerative joint disease characterized by pain, stiffness, and impaired mobility, with current therapies offering limited efficacy. This study investigates the epigenetic role of nuclear receptor-binding SET domain protein 1 (NSD1) in KOA pathogenesis. A KOA mouse model was established, and adenoviral vectors were employed to upregulate Nsd1 and inhibit SRY-box transcription factor 9 (Sox9), followed by histopathological assessments. We examined changes in cell morphology, proliferation, viability, and ferroptosis-related markers. The expression of NSD1, SOX9, and acyl-CoA synthetase long-chain family member 4 (ACSL4) was analyzed, along with the enrichment of NSD1 and dimethylated lysine 36 of histone 3 (H3K36me2) on the SOX9 promoter and SOX9 on the ACSL4 promoter. Additionally, the binding relationship between SOX9 and the ACSL4 promoter sequence was analyzed. Our results revealed that NSD1 expression was reduced in KOA mouse tissues and interleukin-1β-stimulated chondrocytes. NSD1 upregulation alleviated KOA, promoted chondrocyte proliferation and viability, and inhibited ferroptosis. Mechanistically, NSD1 enhanced H3K36me2 to upregulate SOX9 expression, which in turn suppressed ACSL4 expression and ferroptosis. SOX9 inhibition partially reversed the protective effect of NSD1 overexpression. In summary, NSD1 upregulation mitigates chondrocyte ferroptosis and ameliorates KOA by modulating H3K36me2 to upregulate SOX9 and downregulate ACSL4 expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.