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Metabolic Pathway Genes Associated with Susceptibility Genes to Coronary Artery Disease

Overview
Journal Int J Genomics
Publisher Wiley
Date 2018 Apr 3
PMID 29607312
Citations 8
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Abstract

Coronary artery disease (CAD) is one of the leading threats to global health. Previous research has proven that metabolic pathway disorders, such as high blood lipids and diabetes, are one of the risk factors that mostly cause CAD. However, the crosstalk between metabolic pathways and CAD was mostly studied on physiology processes by analyzing a single gene function. A canonical correlation analysis was used to identify the metabolic pathways, which were integrated as a unit to coexpress with CAD susceptibility genes, and to resolve additional metabolic factors that are related to CAD. Seven pathways, including citrate cycle, ubiquinone, terpenoid quinone biosynthesis, and N-glycan biosynthesis, were identified as an integrated unit coexpressed with CAD genes. These pathways could not be revealed as a coexpressed pathway through traditional methods as each single gene has weak correlation. Furthermore, sets of genes in these pathways were candidate markers for diagnosis and detection from patients' serum.

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References
1.
Francke S, Manraj M, Lacquemant C, Lecoeur C, Lepretre F, Passa P . A genome-wide scan for coronary heart disease suggests in Indo-Mauritians a susceptibility locus on chromosome 16p13 and replicates linkage with the metabolic syndrome on 3q27. Hum Mol Genet. 2001; 10(24):2751-65. DOI: 10.1093/hmg/10.24.2751. View

2.
Lee B, Yen C, Hsu H, Lin J, Hsia S, Lin P . A significant correlation between the plasma levels of coenzyme Q10 and vitamin B-6 and a reduced risk of coronary artery disease. Nutr Res. 2012; 32(10):751-6. DOI: 10.1016/j.nutres.2012.09.003. View

3.
Glaros E, Kim W, Quinn C, Wong J, Gelissen I, Jessup W . Glycosphingolipid accumulation inhibits cholesterol efflux via the ABCA1/apolipoprotein A-I pathway: 1-phenyl-2-decanoylamino-3-morpholino-1-propanol is a novel cholesterol efflux accelerator. J Biol Chem. 2005; 280(26):24515-23. DOI: 10.1074/jbc.M413862200. View

4.
McGill Jr H, McMahan C, Gidding S . Preventing heart disease in the 21st century: implications of the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study. Circulation. 2008; 117(9):1216-27. DOI: 10.1161/CIRCULATIONAHA.107.717033. View

5.
Schreiner P, Morrisett J, Sharrett A, Patsch W, Tyroler H, Wu K . Lipoprotein[a] as a risk factor for preclinical atherosclerosis. Arterioscler Thromb. 1993; 13(6):826-33. DOI: 10.1161/01.atv.13.6.826. View