ReviewHeliyon2024
JUN and ATF3 in Gout: Ferroptosis-related potential diagnostic biomarkers.
Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Ferroptosis in gouty arthritis: a potential therapeutic strategy.Frontiers in immunology · 2026Pooled it
- Investigation of the mechanism of Xiaoyin Jiedu Yin in the treatment of psoriasis based on bioinformatics, machine learning.Frontiers in chemistry · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Gout is a prevalent form of chronic inflammatory arthritis, and its etiology remains incompletely understood. Ferroptosis is a form of cell death that relies on iron. As of now, the relationship between ferroptosis and gout is not entirely clear. Hence, the primary objective of this study is to employ bioinformatics methods for the analysis and identification of potential genes associated with ferroptosis in the context of gout. Methods: Utilizing both bioinformatics analysis and machine learning algorithms to systematically identify biomarkers for gout. The gout-related dataset (GSE160170) was acquired from the Gene Expression Omnibus (GEO) database. Ferroptosis-related genes were extracted from the FerrDb database. subsequently, we identified DEGs associated with ferroptosis in the context of gout. Following that, we performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses on the DEGs. Subsequently, SVM-RFE analysis and the LASSO regression model were employed for biomarker screening. Additionally, CIBERSORT software was utilized to assess the composition of twenty-two immune cells in gout, and correlation analyses between hub genes and immune cells were conducted. Results: This study screened a total of twenty-five DEGs related to Ferroptosis in healthy population and gout patient. The KEGG analysis indicates that these DEGs are predominantly enriched in: the AGE-RAGE signaling pathway, nod like receptor signaling pathway, MAPK signaling pathway, IL-17 signaling pathway, etc. The intersection of the top 10 genes identified through PPI network, SVM-RFE analysis, and LASSO regression model resulted in two hub genes, namely JUN and ATF3. Analysis of immunocyte infiltration revealed that JUN exhibited associations with various immune cells, including NK cells resting, Monocytes, Mast cells resting, etc. ATF3, on the other hand, showed associations with immune cells Mast cells resting and Eosinophels. Conclusions: The outcomes of our study pinpointed JUN and ATF3, genes associated with ferroptosis, as promising biomarkers for both diagnosing and treating gout, providing additional evidence to support the important role of ferroptosis in gout and providing potential therapeutic methods for clinical targeted ferroptosis prevention and treatment of gout.
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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 Socratic graph.