ArticleNature communications2020
Osteoclast-associated receptor blockade prevents articular cartilage destruction via chondrocyte apoptosis regulation.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 3 of them syntheses that pooled it.
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
60 citing papers in PubMed, 3 syntheses or guidelines pooled it, 114 citations in OpenAlex.
- [Research progress on the causes of pain in knee osteoarthritis].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026Pooled it
- The causal effect of cytokine cycling levels on osteoarthritis: a bidirectional Mendelian randomized study.Frontiers in immunology · 2023Pooled it
- Pooled it
- Article
- Synovial transcriptional clusters link cartilage degeneration to cell-type-specific gene expression in knee osteoarthritis.bioRxiv : the preprint server for biology · 2026Article
- OSCAR functions as a collagen I receptor to suppress hippo signaling and reprogram lipid metabolism in clear-cell renal cell carcinoma.Cell death & disease · 2026Article
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- Regulated cell death in musculoskeletal development, homeostasis, and diseases.Fundamental research · 2026Review
- Article
- Trojan horse-inspired spatiotemporal strategy augments cartilage regeneration by enhancing mitochondrial energy production.Innovation (Cambridge (Mass.)) · 2025Article
- Starlike Au nanoparticle unleashing siDDIT3 and photothermal power to combat ferroptosis - driven osteoarthritis.Journal of nanobiotechnology · 2025Article
- Suppressive effect of curcumin on apoptosis of articular chondrocytes via regulation on NF-κB pathway and NLRP3 inflammasome.Cytotechnology · 2025Article
- Review
- Signaling Dynamics in Osteogenesis: Unraveling Therapeutic Targets for Bone Generation.Current drug targets · 2025Review
- BCLAF1 Regulates Osteoarthritic Cartilage Degradation Through Interaction with LAMTOR2.International journal of biological sciences · 2025Article
- Epigenetics and Herbs: Potential Therapeutic Strategies for Osteoarthritis of the Knee.Journal of pain research · 2025Review
- Osteoimmunology in Osteoarthritis: Unraveling the Interplay of Immunity, Inflammation, and Joint Degeneration.Journal of inflammation research · 2025Review
- Long non-coding RNAeLife · 2024Article
- Enhancing retention and permeation of rapamycin for osteoarthritis therapy using a two-stage drug delivery system.Materials today. Bio · 2024Article
- Validity evaluation of a rat model of monoiodoacetate-induced osteoarthritis with clinically effective drugs.BMC musculoskeletal disorders · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA), primarily characterized by articular cartilage destruction, is the most common form of age-related degenerative whole-joint disease. No disease-modifying treatments for OA are currently available. Although OA is primarily characterized by cartilage destruction, our understanding of the processes controlling OA progression is poor. Here, we report the association of OA with increased levels of osteoclast-associated receptor (OSCAR), an immunoglobulin-like collagen-recognition receptor. In mice, OSCAR deletion abrogates OA manifestations, such as articular cartilage destruction, subchondral bone sclerosis, and hyaline cartilage loss. These effects are a result of decreased chondrocyte apoptosis, which is caused by the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in induced OA. Treatments with human OSCAR-Fc fusion protein attenuates OA pathogenesis caused by experimental OA. Thus, this work highlights the function of OSCAR as a catabolic regulator of OA pathogenesis, indicating that OSCAR blockade is a potential therapy for OA.
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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.