ArticleArthritis research & therapy2013
Osteopontin - a biomarker for organ damage in paediatric lupus?
Article in Arthritis research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 4 citations in OpenAlex.
- Association of the osteopontin rs1126616 polymorphism and a higher serum osteopontin level with lupus nephritis.Biomedical reports · 2016Article
- Adipokines, biomarkers of endothelial activation, and metabolic syndrome in patients with ankylosing spondylitis.BioMed research international · 2014Review
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing body of literature has demonstrated that the multifunctional glycoprotein osteopontin (OPN), has a role in type I interferon (IFN) production and may be involved in systemic lupus erythematosus (SLE) pathogenesis. A recent report has provided further support for this, demonstrating an association between raised baseline circulating plasma osteopontin (cOPN) levels and IFN, and an elevation in cOPN prior to the onset of both increased cumulative disease and end-organ damage. These associations were most marked in paediatric SLE, implying that cOPN may be a useful biomarker of disease activity in childhood lupus.
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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.