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Erdmann, J., Grosshennig, A., Braund, P.S., Konig, I.R., Hengstenberg, C., Hall, A.S., Linsel-Nitschke, P., Kathiresan, S., Wright, B., Tregouet, D.A., Cambien, F., Bruse, P., Aherrahrou, Z., Wagner, A.K., Stark, K., Schwartz, S.M., Salomaa, V., Elosua, R., Melander, O., Voight, B.F., O’Donnell, C.J., Peltonen, L., Siscovick, D.S., Altshuler, D., Merlini, P.A., Peyvandi, F., Bernardinelli, L., Ardissino, D., Schillert, A., Blankenberg, S., Zeller, T., Wild, P., Schwarz, D.F., Tiret, L., Perret, C., Schreiber, S., El Mokhtari, N.E., Schafer, A., Marz, W., Renner, W., Bugert, P., Kluter, H., Schrezenmeir, J., Rubin, D., Ball, S.G., Balmforth, A.J., Wichmann, H.E., Meitinger, T., Fischer, M., Meisinger, C., Baumert, J., Peters, A., Ouwehand, W.H., Deloukas, P., Thompson, J.R., Ziegler, A., Samani, N.J. and Schunkert, H. (2009) New susceptibility locus for coronary artery disease on chromosome 3q22.3. Nature Genetics, 41, 280-282. doi:10.1038/ng.307
has been cited by the following article:
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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.
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