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Related Experiment Video

Updated: Feb 7, 2026

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Epigenetics in Abdominal Aortic Aneurysm: Mechanisms and Risk Prediction.

Shuai Yuan1,2,3,4, Gabrielle Shakt1,2, Michael G Levin1,5

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Summary

This study identified DNA methylation markers linked to abdominal aortic aneurysm (AAA) risk. These findings highlight inflammatory pathways, blood lipids, and immune proteins as key contributors to AAA development.

Keywords:
DNA methylationabdominal aortic aneurysmepigeneticsmechanismprediction

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Area of Science:

  • Genetics and Genomics
  • Epigenetics
  • Cardiovascular Disease Research

Background:

  • The epigenetic mechanisms influencing susceptibility to abdominal aortic aneurysm (AAA) are not well understood.
  • Identifying causal DNA methylation markers for AAA is crucial for understanding aneurysm formation and developing translational applications.

Purpose of the Study:

  • To identify DNA methylation biomarkers associated with abdominal aortic aneurysm (AAA) using the VA Million Veteran Program (MVP).
  • To elucidate the underlying molecular pathways and genetic regulatory processes driving AAA development.

Main Methods:

  • Conducted an epigenome-wide association study (EWAS) of incident AAA.
  • Utilized Mendelian randomization (MR) for causal inference of CpG-AAA associations.
  • Integrated multi-omics data, including transcriptional data and expression quantitative trait methylation (eQTM), for pathway analysis.
  • Developed and evaluated a methylation-based risk predictor model.

Main Results:

  • Identified 1,253 CpGs associated with incident AAA, with 151 supported by MR as putatively causal.
  • Functional annotation revealed enrichment of inflammatory transcription factor programs (e.g., AP-1) and predominantly distal enhancer regulation.
  • Network MR implicated 231 mediation pathways, including cardiometabolic traits (e.g., blood lipids) and immune/inflammation-related traits (e.g., platelet count, specific proteins).
  • A methylation risk score improved AAA prediction accuracy when added to a clinical model.

Conclusions:

  • Identified putative causal DNA methylation markers for AAA.
  • Multi-omics analyses implicate AP-1-linked inflammatory programs, blood lipids, platelet count, and immune proteins in AAA pathogenesis.
  • These findings provide insights into methylation-associated AAA risk pathways and potential therapeutic targets.