ArticleFrontiers in pharmacology2025
Asperosaponin VI suppresses ferroptosis in chondrocytes and ameliorates osteoarthritis by modulating the Nrf2/GPX4/HO-1 signaling pathway.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Asperosaponin VI Ameliorates Spontaneous Abortion by Inhibiting Trophoblast Ferroptosis via the KEAP1/NRF2/GPX4 Axis.Antioxidants (Basel, Switzerland) · 2026Article
- Targeting Ferroptosis With Natural Products for the Treatment of Skeletal System Disease: An Updated Review.Journal of cellular and molecular medicine · 2026Review
- Nrf2 as a redox checkpoint in autoimmune joint inflammation: microenvironmental redox control across the arthritis spectrum.Frontiers in immunology · 2026Review
- Study on the analgesic and anti-inflammatory mechanisms of Jingu Zhitong gel in the treatment of knee osteoarthritis through the IL-17, NGF-TrkA, and COX-2/PGE2 pathways.Frontiers in pharmacology · 2026Article
- The Nrf2/HO-1 signaling pathway in arthritis: from molecular mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Research progress on the mechanism of chondrocyte ferroptosis in osteoarthritis.Frontiers in immunology · 2026Review
- Role and mechanism of lncRNA ZEB1-AS1 endogenous competition for miR-365a-3p targeting NRF2 in ferroptosis in articular chondrocytes.Journal of molecular histology · 2025Article
- Glutathione peroxidase 4 as an emerging therapeutic target in osteoarthritis: focus on ferroptosis.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Asperosaponin VI (AVI) is a naturally occurring monosaccharide derived from Objective: To elucidate the specific mechanism through which AVI affects chondrocytes in osteoarthritis (OA). Methods: For the Results: AVI alleviated chondrocyte apoptosis and extracellular matrix degradation in rat OA induced by IL-1β. It attenuated the levels of TNF-α, IL-6, and PGE2 while reducing those of Fe Conclusion: Our findings suggest that AVI is a promising therapeutic agent for OA. It exerted its protective effect by regulating the Nrf2/GPX4/HO-1 signaling axis to inhibit cartilage cell ferroptosis and improve osteoarthritis.
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Registered trials
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