ArticleAnnals of the rheumatic diseases2020
TRIM24-RIP3 axis perturbation accelerates osteoarthritis pathogenesis.
Article in Annals of the rheumatic diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 84 citations in OpenAlex.
- TIF1 Family Proteins as Modulators of Cell Death: Mechanisms and Therapeutic Opportunities.Biomolecules · 2026Review
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- Research Prospects for Necroptosis in Inflammatory Diseases: A Bibliometric Analysis.Current medicinal chemistry · 2026Review
- Regulated cell death in musculoskeletal development, homeostasis, and diseases.Fundamental research · 2026Review
- RIPK3 is spatially associated with cartilage degeneration in osteoarthritis: integrative transcriptomic and histological analysis.Journal of orthopaedic surgery and research · 2025Article
- Benchmarking of dimensionality reduction methods to capture drug response in transcriptome data.Scientific reports · 2025Article
- Magnetic Nanoparticles Combined With Pulsed Electromagnetic Field Alleviate Chondrocyte Necroptosis in Osteoarthritis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Integrative transcriptomic analysis identifies emetine as a promising candidate for overcoming acquired resistance to ALK inhibitors in lung cancer.Molecular oncology · 2025Article
- Blockade of ZMIZ1-GATA4 Axis Regulation Restores Youthfulness to Aged Cartilage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Comprehensive Analysis of Programmed Cell Death-Related Genes in Diagnosis and Synovitis During Osteoarthritis Development: Based on Bulk and Single-Cell RNA Sequencing Data.Journal of inflammation research · 2025Article
- Acetyl-11-keto-beta-boswellic acid ameliorates monosodium iodoacetate-induced osteoarthritis in rats: implications of HMGB1/TLR4/NF-κB and Nrf2/HO-1.Frontiers in pharmacology · 2025Article
- AZ-628 sensitizes donafenib in hepatocellular carcinoma by targeting tyrosine kinase pathway and ferroptosis.CytoJournal · 2025Article
- Epigenetics and Herbs: Potential Therapeutic Strategies for Osteoarthritis of the Knee.Journal of pain research · 2025Review
- Thrombospondin-1 mitigates osteoarthritis progression by inhibiting mechanical stress-induced chondrocyte ferroptosis via the integrin/YAP pathway.Frontiers in immunology · 2025Article
- Article
- An intra articular injectable Mitocelle recovers dysfunctional mitochondria in cellular organelle disorders.Bioactive materials · 2025Article
- RIP1 inhibition reduces chondrocyte apoptosis through downregulating nuclear factor-kappa B signaling in a mouse osteoarthritis model.Molecular biology reports · 2024Article
- Significance of Necroptosis in Cartilage Degeneration.Biomolecules · 2024Review
- Screening chondrocyte necroptosis-related genes in the diagnosis and treatment of osteoarthritis.Heliyon · 2024Article
- FTH1 protects against osteoarthritis by MAPK pathway inhibition of extracellular matrix degradation.BMC musculoskeletal disorders · 2024Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesRecently, necroptosis has attracted increasing attention in arthritis research; however, it remains unclear whether its regulation is involved in osteoarthritis (OA) pathogenesis. Since receptor-interacting protein kinase-3 (RIP3) plays a pivotal role in necroptosis and its dysregulation is involved in various pathological processes, we investigated the role of the RIP3 axis in OA pathogenesis.
methodsExperimental OA was induced in wild-type or
resultsRIP3 expression was markedly higher in damaged cartilage from patients with OA than in undamaged cartilage. In the mouse model, adenoviral RIP3 overexpression accelerated cartilage disruption, whereas
conclusionsTRIM24-RIP3 axis perturbation promotes OA chronicity by activating RIP3 kinase, suggesting that the therapeutic manipulation of this pathway could provide new avenues for treating OA.
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