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Key genes of the interleukin 6 signaling pathway are not associated with coronary artery disease in a large European population

Author(s): Mark Luedde | Arne S. Schaefer | Natalie Scheller | Corinna Doege | Hans-Joerg Hippe | Michael Nothnagel | Nils Haake | Norbert Frey | Stefan Schreiber | Nour Eddine El-Mokhtari

Journal: Open Journal of Genetics
ISSN 2162-4453

Volume: 03;
Issue: 01;
Start page: 67;
Date: 2013;
Original page

Keywords: Coronary Artery Disease | Genetics | Single Nucleotide Polymorphism | Interleukin 6

Background: Recent studies indicate a strong functional relevance of the canonical inflammatory interleukin 6 signaling pathway in coronary artery disease (CAD). A genetic association of this signaling pathway with CAD has not been shown yet. We aimed to assess novel single nucleotide polymorphisms (SNPs) from genes of the Interleukin 6 signaling pathway. Results: To identify novel SNPs that are relevant for CAD, we employed a large-scale population-based case-control association study of 2199 cases and 1715 controls and assessed 73 SNPs from 12 genes out of the IL-6 signaling pathway. Results were adjusted to the CAD-related risk factors diabetes, hypertension, Body Mass Index, smoking and sex by logistic regression analysis. In a primary explorative study, we identified 5 SNPs that were significantly associated with CAD (MAPK1_rs6928, MAPK1_rs9340, MAPK1_ rs11913721, MAPK14_rs7757672, JAK1_rs310236). After adjustment to CAD-risk factors, MAPK1_ rs6928 showed the strongest association with CAD (P 0.0217, Odds Ratio 1.36, Confidence Interval 1.05 - 1.77). To reproduce this result, we performed a replication study employing independent patient and control panels. In this study we could not approve the association of rs6928 with CAD. Conclusion: In conclusion, we did not detect significant associations of SNPs from the IL-6 signaling pathway with CAD. Our investigation demonstrates the importance of independent replication studies to verify results from candidate-gene association studies in the quest to discover the underlying pathomechanism of CAD.
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