Genetic variations in PADI4 and CCR6: a comprehensive meta-analysis on rheumatoid arthritis susceptibility
Background Rheumatoid arthritis is a long-term autoimmune condition that causes damage and inflammation to the joints. Genetic factors, including polymorphisms in the PADI4 and CCR6 genes, contribute significantly to RA susceptibility. Methods To find research on RA, PADI4 , CCR6 , gene polymorphism...
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Veröffentlicht in: | Egyptian Journal of Medical Human Genetics 2024-09, Vol.25 (1), p.108-11, Article 108 |
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Sprache: | eng |
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Zusammenfassung: | Background
Rheumatoid arthritis is a long-term autoimmune condition that causes damage and inflammation to the joints. Genetic factors, including polymorphisms in the
PADI4
and
CCR6
genes, contribute significantly to RA susceptibility.
Methods
To find research on RA,
PADI4
,
CCR6
, gene polymorphisms, and SNPs, we performed a meta-analysis using PubMed, Scopus, Medline, Google Scholar, and EMBASE. Inclusion criteria comprised case–control studies providing genotypic data and allele frequencies. Review Manager 5.4 was used to conduct statistical analysis and evaluate odds ratios with 95% confidence intervals.
Results
Heterogeneity analyses of
CCR6
rs3093024 showed no significant associations across genetic models: allele (OR = 0.69, 95% CI [0.36–1.32]), homozygous (OR = 2.18, 95%CI [0.58–8.22]), heterozygous (OR = 0.60, 95% CI [0.31–1.16]), dominant (OR = 1.60, 95% CI [0.64–3.95]), and recessive (OR = 1.79, 95% CI [0.75–4.27]). Similarly,
PADI4
rs1748033 and rs2240340 showed insignificant associations across all genetic models.
Conclusion
This meta-analysis identifies a substantial relationship between
CCR6
rs3093024 and RA susceptibility in Asian populations. However, heterogeneity analyses indicate inconsistent associations for
PADI4
rs1748033 and rs2240340 across different populations and genetic models, suggesting varied genetic influences. Further large-scale studies are required to confirm these results and investigate the complex genetic and environmental interactions underlying RA pathogenesis. |
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ISSN: | 2090-2441 1110-8630 2090-2441 |
DOI: | 10.1186/s43042-024-00550-1 |