TET2: A Novel Epigenetic Regulator and Potential Intervention Target for Atherosclerosis

DNA Cell Biol. 2018 Jun;37(6):517-523. doi: 10.1089/dna.2017.4118. Epub 2018 Apr 13.

Abstract

Atherosclerosis is the underlying cause of cardio-cerebrovascular disease. However, the mechanisms of atherosclerosis are still unclear. The modification of DNA methylation has an important role in atherosclerosis development. As a member of the Ten-eleven translocation (TET) family, TET methylcytosine dioxygenase 2 (TET2) can modify DNA methylation by catalyzing 5-methylcytosine to 5-hydroxymethylcytosine and mediate DNA demethylation. Recent findings suggest that TET2 is related to the phenotype transformation of vascular smooth muscle cells, endothelial dysfunction, and inflammation of macrophage, the key factors of atherosclerosis. Therefore, TET2 may be a potential target for atherosclerosis treatment. This review will elaborate the recent findings that suggest the role of TET2 in atherosclerosis.

Keywords: DNA demethylation; TET2; atherosclerosis; inflammation.

Publication types

  • Review

MeSH terms

  • Atherosclerosis / genetics*
  • Atherosclerosis / metabolism
  • DNA Methylation*
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Dioxygenases
  • Endothelial Cells / metabolism
  • Epigenesis, Genetic*
  • Gene Expression Regulation
  • Humans
  • Inflammation / genetics
  • Inflammation / metabolism
  • Muscle, Smooth, Vascular / cytology
  • Myocytes, Smooth Muscle / metabolism
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins / metabolism

Substances

  • DNA-Binding Proteins
  • Proto-Oncogene Proteins
  • Dioxygenases
  • TET2 protein, human