In a recent genome-wide association study, the zinc finger, C3HC-type containing 1 (ZC3HC1) polymorphism was strongly associated with coronary artery disease (CAD) by an unknown mechanism. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is related with CAD through low-density lipoprotein (LDL) metabolism. The association of both of the above genetic variants with hypertension was studied in a Finnish 50-year-old cohort.A total of 325 hypertensive cases and 444 nonhypertensive controls were obtained from the Tampere adult population cardiovascular risk study. Samples were genotyped for ZC3HC1 rs11556924 and PCSK9 rs11206510 polymorphisms using Competitive Allele Specific PCR technique. A subpopulation that had available follow-up data from ages of 40, 45, and 50 years was also analyzed.ZC3HC1 rs11556924 (C > T) genotype CC was associated with hypertension compared with the T-allele carriers (P = 0.013). PCSK9 rs11206510 (T > C) genotype was not associated with hypertension. Its major TT-genotype was associated with higher total cholesterol (P = 0.044) and LDL (P = 0.029) compared with the C-allele.We report for the first time that ZC3HC1 rs11556924 was associated with essential hypertension in 50-year-old patients. Although PCSK9 rs11206510 was not associated with hypertension, our study confirms its association with serum cholesterol levels.
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http://dx.doi.org/10.1097/MD.0000000000001221 | DOI Listing |
Rev Cardiovasc Med
September 2021
Department of Nutrition and Food Hygiene, School of Public Health, China Medical University, 110122 Shenyang, Liaoning, China.
Hypertension is a complex disease which is mainly influenced by genetic factors. Recently, genome-wide association study (GWAS) found three novel endothelial dysfunction-related sites: Vascular endothelial growth factor A () rs9472135, Faciogenital dysplasia 5 () rs11128722, Zinc Finger C3HC-type Containing 1 () rs11556924. Endothelial dysfunction is one of the early events in pathophysiology of essential hypertension.
View Article and Find Full Text PDFCrit Rev Eukaryot Gene Expr
August 2020
Dept. of Medical Genetics, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Medical Genetic Research Center (MGRC), School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Academic Center for Education, Culture, and Research (ACECR)-Khorasan Razavi, Mashhad, Iran.
Coronary artery disease (CAD) and ischemic stroke (IS) are commonly considered distinct disease phenotypes. However, there is some evidence in favor of a degree of overlap between genetic susceptibility to CAD and genetic risk factors for IS. In the present study, we aimed to examine the role of two single-nucleotide polymorphisms (SNPs), rs3825807 and rs11556924, located in the ADAMTS7 and ZC3HC1 genes, respectively, associated with CAD in published GWASs in European populations and their possible contribution to the development of coronary atherosclerosis and cerebral LA atherosclerosis in a case-control study of an the Iranian population.
View Article and Find Full Text PDFCurr Mol Med
November 2021
Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Soochow University, Suzhou, Jiangsu 215123, China.
Purpose: Phosphorylation-related SNP (phosSNP) is a non-synonymous SNP that might influence protein phosphorylation status. The aim of this study was to assess the effect of phosSNPs on blood pressure (BP), coronary artery disease (CAD) and ischemic stroke (IS).
Methods: We examined the association of phosSNPs with BP, CAD and IS in shared data from genome-wide association studies (GWAS) and tested if the disease loci were enriched with phosSNPs.
Circ Cardiovasc Genet
January 2017
From the Atherogenomics Laboratory, University of Ottawa Heart Institute, Canada.
J Biol Chem
July 2016
From the Department of Cardiovascular Sciences and NIHR Leicester Cardiovascular Biomedical Research Unit, Glenfield Hospital, University of Leicester, Leicester, LE3 9QP and
Genome-wide association studies have to date identified multiple coronary artery disease (CAD)-associated loci; however, for most of these loci the mechanism by which they affect CAD risk is unclear. The CAD-associated locus 7q32.2 is unusual in that the lead variant, rs11556924, is not in strong linkage disequilibrium with any other variant and introduces a coding change in ZC3HC1, which encodes NIPA.
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