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Can J Cardiol. 2012 Nov-Dec;28(6):662-6. doi: 10.1016/j.cjca.2012.05.014. Epub 2012 Aug 15.

Inflammation and coronary artery disease: insights from genetic studies.

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1
University of Ottawa Heart Institute, Ottawa, Ontario, Canada. rmcpherson@ottawaheart.ca

Abstract

Recent genome-wide association studies (GWASs) have provided a vast amount of new information relevant to the myriad of biological pathways related to atherosclerosis and its progression. Although atherosclerosis is a complex process, both GWASs and candidate gene studies add support to the hypothesis that proinflammatory pathways, involving both innate and adaptive immunity, play a causal role in coronary artery disease (CAD) and its clinical manifestations. Recent GWASs have identified several inflammation-related loci associated with CAD risk. These include CXCL2, encoding an atheroprotective chemokine, and a region near HLA-C in the major histocompatibility locus on chromosome 6p21. The ABO locus, also linked to CAD risk by the GWAS approach, is related to multiple phenotypes, including plasma interleukin-6 (IL-6) levels. Finally, relevant to inflammation, the 9p21 CAD risk locus appears to play a role in interferon-gamma signalling. Candidate gene studies also support a causative role of inflammation pathways in atherosclerosis. Of note, a common loss of function coding variant in the IL-6 receptor gene (IL6R) is associated with a reduction in CAD risk.

PMID:
22902153
DOI:
10.1016/j.cjca.2012.05.014
[Indexed for MEDLINE]
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