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Tregouet, D.A., Konig, I.R., Erdmann, J., Munteanu, A., Braund, P.S., Hall, A.S., Grosshennig, A., LinselNitschke, P., Perret, C., DeSuremain, M., Meitinger, T., Wright, B.J., Preuss, M., Balmforth, A.J., Ball, S.G., Meisinger, C., Germain, C., Evans, A., Arveiler, D., Luc, G., Ruidavets, J.B., Morrison, C., van der Harst, P., Schreiber, S., Neureuther, K., Schafer, A., Bugert, P., El Mokhtari, N.E., Schrezenmeir, J., Stark, K., Rubin, D., Wichmann, H.E., Hengstenberg, C., Ouwehand, W., Ziegler, A., Tiret, L., Thompson, J.R., Cambien, F., Schunkert, H. and Samani, N.J. (2009) Genome-wide haplotype association study identifies the SLC22A3-LPAL2-LPA gene cluster as a risk locus for coronary artery disease. Nature Genetics, 41, 283-285. doi:10.1038/ng.314

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

  AUTHORS: Mark Luedde, Arne S. Schaefer, Natalie Scheller, Corinna Doege, Hans-Joerg Hippe, Michael Nothnagel, Nils Haake, Norbert Frey, Stefan Schreiber, Nour Eddine El-Mokhtari

  KEYWORDS: Coronary Artery Disease; Genetics; Single Nucleotide Polymorphism; Interleukin 6

  JOURNAL NAME: Open Journal of Genetics, Vol.3 No.1, March 29, 2013

  ABSTRACT: 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.