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DNA methylation modules associate with incident cardiovascular disease and cumulative risk factor exposure.

Abstract：

BACKGROUND:Epigenome-wide association studies using DNA methylation have the potential to uncover novel biomarkers and mechanisms of cardiovascular disease (CVD) risk. However, the direction of causation for these associations is not always clear, and investigations to-date have often failed to replicate at the level of individual loci. METHODS:Here, we undertook module- and region-based DNA methylation analyses of incident CVD in the Women's Health Initiative (WHI) and Framingham Heart Study Offspring Cohort (FHS) in order to find more robust epigenetic biomarkers for cardiovascular risk. We applied weighted gene correlation network analysis (WGCNA) and the Comb-p algorithm to find methylation modules and regions associated with incident CVD in the WHI dataset. RESULTS:We discovered two modules whose activation correlated with CVD risk and replicated across cohorts. One of these modules was enriched for development-related processes and overlaps strongly with epigenetic aging sites. For the other, we showed preliminary evidence for monocyte-specific effects and statistical links to cumulative exposure to traditional cardiovascular risk factors. Additionally, we found three regions (associated with the genes SLC9A1, SLC1A5, and TNRC6C) whose methylation associates with CVD risk. CONCLUSIONS:In sum, we present several epigenetic associations with incident CVD which reveal disease mechanisms related to development and monocyte biology. Furthermore, we show that epigenetic modules may act as a molecular readout of cumulative cardiovascular risk factor exposure, with implications for the improvement of clinical risk prediction.

journal_name

Clin Epigenetics

journal_title

Clinical epigenetics

authors

Westerman K,Sebastiani P,Jacques P,Liu S,DeMeo D,Ordovás JM

doi

10.1186/s13148-019-0705-2

subject

Has Abstract

pub_date

2019-10-15 00:00:00

pages

142

issue

1

eissn

1868-7075

issn

1868-7083

pii

10.1186/s13148-019-0705-2

journal_volume

11

pub_type

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