ReviewBiomolecules2024
Significance of Necroptosis in Cartilage Degeneration.
Review in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed.
- Endocrine‑metabolic imbalance drives osteoarthritis: From whole‑joint pathobiology to precision therapy (Review).International journal of molecular medicine · 2026Review
- USP39 inhibits MLKL phosphorylation and deubiquitination to suppress necroptosis of nucleus pulposus cells and attenuate intervertebral disc degeneration.Journal of orthopaedic translation · 2026Article
- Focus on necroptosis: its role in the pathogenesis and therapeutic potential of osteoarthritis.Frontiers in immunology · 2026Review
- Frontier research on mechanisms of bone destruction in rheumatoid arthritis.Frontiers in cell and developmental biology · 2026Review
- Propionate attenuates osteoarthritis progression by regulating the gut-joint axis.Frontiers in immunology · 2026Article
- TMEM164 enhances radioresistance of GBM cells by inhibiting the FASN-NADPH-ROS axis.Journal of neuro-oncology · 2025Article
- RIPK3 is spatially associated with cartilage degeneration in osteoarthritis: integrative transcriptomic and histological analysis.Journal of orthopaedic surgery and research · 2025Article
- Targeting the senescence-associated secretory phenotype to modify osteoarthritis in aging.Inflammopharmacology · 2025Review
- Cuproptosis in osteoarthritis: Exploring chondrocyte cuproptosis and therapeutic avenues.Journal of orthopaedic translation · 2025Article
- Andrographolide prevents necroptosis by suppressing the generation of reactive oxygen species.Acta biochimica et biophysica Sinica · 2025Article
- Core autophagy genes and immune infiltration characteristics in rheumatoid arthritis: A bioinformatics study.PloS one · 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
- Types of cell death in diabetic cardiomyopathy: insights from animal models.Acta biochimica et biophysica Sinica · 2024Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Cartilage, a critical tissue for joint function, often degenerates due to osteoarthritis (OA), rheumatoid arthritis (RA), and trauma. Recent research underscores necroptosis, a regulated form of necrosis, as a key player in cartilage degradation. Unlike apoptosis, necroptosis triggers robust inflammatory responses, exacerbating tissue damage. Key mediators such as receptor-interacting serine/threonine-protein kinase-1 (RIPK1), receptor-interacting serine/threonine-protein kinase-3(RIPK3), and mixed lineage kinase domain-like (MLKL) are pivotal in this process. Studies reveal necroptosis contributes significantly to OA and RA pathophysiology, where elevated RIPK3 and associated proteins drive cartilage degradation. Targeting necroptotic pathways shows promise; inhibitors like Necrostatin-1 (Nec-1), GSK'872, and Necrosulfonamide (NSA) reduce necroptotic cell death, offering potential therapeutic avenues. Additionally, autophagy's role in mitigating necroptosis-induced damage highlights the need for comprehensive strategies addressing multiple pathways. Despite these insights, further research is essential to fully understand necroptosis' mechanisms and develop effective treatments. This review synthesizes current knowledge on necroptosis in cartilage degeneration, aiming to inform novel therapeutic approaches for OA, RA, and trauma.
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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 OpenQuestion graph.