ArticleScientific reports2024
Causal relationship between inflammatory proteins, immune cells, and gout: a Mendelian randomization study.
Article in Scientific reports, 2024. 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.
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Who cites it
2 citing papers in PubMed.
- A Predictive Model of Cardiovascular Aging by Clinical and Immunological Markers Using Machine Learning.Diagnostics (Basel, Switzerland) · 2025Article
- Exploring Immunological Determinants and Constructing a Predictive Model for for Diagnosis of Gout: Insights Into Immune Biomarkers.Journal of inflammation research · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prior research has documented the association between certain circulating inflammatory proteins/immune cells and gout. However, the reliability of these associations remains contentious due to the constraints of conventional observational methodologies. This investigation seeks to reassess the causative link between circulating inflammatory proteins/immune cells and gout through the application of Mendelian randomization (MR). The study included 3576 individuals of European ancestry with gout, immune cell data from the GWAS summary of 3757 Sardinians, and circulating inflammatory protein data from 14,824 European ancestry participants for MR analysis. The principal approach employed was inverse variance weighted analysis to investigate the causal relationship between exposure and outcomes. The results indicate that CD28 on CD39+ CD4+ T cells may be associated with a reduced risk of gout. Additionally, CD45RA+ CD28- CD8bright T cells may also be associated with a reduced risk of gout. In contrast, DN (CD4-CD8-) T cells and IL-12β may increase the risk of gout. Some inflammatory proteins and immune cells show potential causal associations with gout. Nevertheless, additional experimental verification is warranted to assess the underlying mechanisms and confirm the causative role of these immune factors in gout pathogenesis.
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Registered trials
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