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DNA Methylation Aberrant in Atherosclerosis.

Yao Dai1, Danian Chen1, Tingting Xu1

  • 1Department of Cardiology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

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|March 21, 2022
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Summary
This summary is machine-generated.

DNA methylation plays a key role in atherosclerosis (AS) development. This review explores how DNA methylation changes with age and oxidative stress, offering potential epigenetic treatment targets for AS.

Keywords:
DNA methylationagingatherosclerosishyperhomocysteinemiaoxidative stress

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Area of Science:

  • Cardiovascular Biology
  • Epigenetics
  • Molecular Medicine

Background:

  • Atherosclerosis (AS) involves lipid oxidation, immune activation, and endothelial dysfunction, exacerbated by aging and hyperhomocysteinemia.
  • Epigenetic modifications, particularly DNA methylation, are crucial in AS pathogenesis, mediating environmental influences on gene expression.
  • The precise relationship between AS progression and DNA methylation patterns remains incompletely elucidated.

Purpose of the Study:

  • To review abnormal DNA methylation changes in atherosclerosis.
  • To explore the influence of aging, methyl supply, and oxidative stress on DNA methylation in AS.
  • To summarize current epigenetic treatment strategies for AS.

Main Methods:

  • Literature review of studies on DNA methylation and atherosclerosis.
  • Analysis of age-related genome-wide hypermethylation in AS.
  • Investigation of hyperhomocysteinemia's link to methylation and oxidative stress's effect on demethylation via TET proteins.

Main Results:

  • Genome-wide hypermethylation is prevalent in aging-associated AS.
  • Hypermethylation is linked to methyl supply, contributing to hyperhomocysteinemia.
  • Oxidative stress interferes with TET protein function, impacting demethylation processes.

Conclusions:

  • DNA methylation alterations are central to AS pathogenesis.
  • Understanding these epigenetic changes offers insights into AS progression.
  • Epigenetic therapies present promising new therapeutic avenues for atherosclerosis.