ArticleBioMed research international2013
Phosphocitrate is potentially a disease-modifying drug for noncrystal-associated osteoarthritis.
Article in BioMed research international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Focus on the NLRP3 inflammasome: its role in the pathogenesis and therapeutic potential of inflammation-driven osteoarthritis.Frontiers in immunology · 2026Review
- Targeting inflammasome-dependent mechanisms as an emerging pharmacological approach for osteoarthritis therapy.iScience · 2022Review
- An animal model study on the gene expression profile of meniscal degeneration.Scientific reports · 2020Article
- The role of inhibition by phosphocitrate and its analogue in chondrocyte differentiation and subchondral bone advance in Hartley guinea pigs.Experimental and therapeutic medicine · 2018Article
- Biological Effects of Phosphocitrate on Osteoarthritic Articular Chondrocytes.The open rheumatology journal · 2017Article
- Sodium Thiosulfate Prevents Chondrocyte Mineralization and Reduces the Severity of Murine Osteoarthritis.PloS one · 2016Article
- Disease-modifying effects of phosphocitrate and phosphocitrate-β-ethyl ester on partial meniscectomy-induced osteoarthritis.BMC musculoskeletal disorders · 2015Article
- Expression of phosphocitrate-targeted genes in osteoarthritis menisci.BioMed research international · 2014Article
- Biological activities of phosphocitrate: a potential meniscal protective agent.BioMed research international · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phosphocitrate (PC), a calcification inhibitor, inhibits the development of crystal-associated osteoarthritis (OA) in Hartley guinea pigs. However, the molecular mechanisms underlying its disease-modifying effect remain elusive. This study sought to test the hypothesis that PC has calcium crystal-independent biological activities which are, at least in part, responsible for its disease-modifying activity. We found that PC inhibited the proliferation of OA fibroblast-like synoviocytes in the absence of calcium crystals. Consistent with its effect on cell proliferation, PC downregulated the expression of numerous genes classified in cell proliferation. PC also downregulated the expression of many genes classified in angiogenesis and inflammatory response including prostaglandin-endoperoxide synthase 2, interleukin-1 receptor, type I, and chemokine (C-C motif) ligand 2. In contrast, PC upregulated the expression of many genes classified in musculoskeletal tissue development, including aggrecan, type I collagen, and insulin-like growth factor binding protein 5. These findings suggest that PC is not only a promising disease-modifying drug for crystal-associated OA but also for noncrystal-associated 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.