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- W3176150205 abstract "DNA methylation is an ideal biomarker for many applications, because it has both the stability for prognostic use and the plasticity to be altered by environmental variables including diet. Investigations of relationships between DNA methylation and cardiovascular disease (CVD) have been performed, but these cross-sectional analyses are susceptible to reverse causation, making causal inference difficult. Thus, we hypothesized that analysis of methylation in large-scale cohorts with follow-up for CVD development could provide potential risk biomarkers as well as mechanistic insights into disease risk. We performed an epigenome-wide association study for incident CVD in individuals from the Framingham Heart Study Offspring Cohort and Women's Health Initiative studies. Methylation data were previously collected from whole blood samples using the Illumina Infinium HumanMethylation450k platform. Cox regression methods were used to identify relationships between relative methylation levels and incident CVD both at specific CpG sites and using a region-based approach. We identified 10 single CpG sites and 4 regions demonstrating suggestive associations with incident CVD. Mendelian randomization approaches provided preliminary evidence of a causal relationship between methylation within the APOB gene and CVD. Investigations of cell-type specific relationships using available epigenomic annotations highlighted the importance of monocytes in mediating the risk captured by methylation data in blood. Finally, relationships between these CpG sites and known traditional cardiovascular risk factors were examined to understand how they might interact to increase CVD risk. Based on these results, DNA methylation may provide a useful complement to existing cardiovascular risk prediction methods, and provides insights into genomic processes that may mediate the effects of genetics and environmental factors on disease risk. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal." @default.
- W3176150205 created "2021-07-05" @default.
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- W3176150205 date "2018-04-01" @default.
- W3176150205 modified "2023-10-18" @default.
- W3176150205 title "Epigenome‐Wide Association Study of Incident Cardiovascular Disease" @default.
- W3176150205 doi "https://doi.org/10.1096/fasebj.2018.32.1_supplement.lb114" @default.
- W3176150205 hasPublicationYear "2018" @default.
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