PMID- 31116040
OWN - NLM
STAT- MEDLINE
DCOM- 20191104
LR  - 20191104
IS  - 2169-141X (Electronic)
IS  - 2169-1401 (Linking)
VI  - 47
IP  - 1
DP  - 2019 Dec
TI  - DNA methylation abnormalities in atherosclerosis.
PG  - 2031-2041
LID - 10.1080/21691401.2019.1617724 [doi]
AB  - Atherosclerosis is a complex disease with involvement of intermediate-, 
      large-sized arteries. Atherosclerosis is characterized by the accumulation of 
      vascular lipids, immune system activation, inflammation, oxidative stress and 
      oxidized low-density lipoproteins (LDLs), endothelial cell (EC) activation, 
      arterial smooth muscle cell (SMC) proliferation, macrophage activation and foam 
      cell formation that cause endothelial dysfunction. DNA methylation is one of 
      important epigenetic mechanisms which changes gene expression. It has been 
      evident that this mechanism plays an important role in the initiation and 
      propagation of atherosclerosis. Furthermore, DNA methylation is a crucial and 
      distinct mechanism that modulates genes governing cell proliferation, thereby 
      connecting environmental insults with gene expression. This study represents many 
      atherosclerosis-related genes which are regulated through DNA methylation 
      mechanism. Although the role of epigenetics in atherosclerosis is at their 
      infancy. Nevertheless, various studies demonstrated that DNA methylation 
      involvement in this disease is undeniable. DNA methyltransferases are the main 
      player of the smooth muscle cell proliferation, endothelial cell integrity, as 
      well as arteriosclerosis formation. In this review, we focus on recent 
      achievements in the functional and description interpretation of the DNA 
      methylation pattern of cells and tissues implicated in atherosclerosis. Besides, 
      we discuss the association of DNA methylation with oxidative stress, 
      hyperhomocysteinemia (HHcy), ageing, and inflammation in the development and 
      pathogenesis of atherosclerosis.
FAU - Tabaei, Samira
AU  - Tabaei S
AD  - a Department of Immunology, School of Medicine, Shiraz University of Medical 
      Sciences , Shiraz , Iran.
FAU - Tabaee, Seyyedeh Samaneh
AU  - Tabaee SS
AD  - b Department of Cardiology, Neyshabur University of Medical Science , Neyshabur , 
      Iran.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Artif Cells Nanomed Biotechnol
JT  - Artificial cells, nanomedicine, and biotechnology
JID - 101594777
SB  - IM
MH  - Aging/genetics
MH  - Animals
MH  - Atherosclerosis/complications/*genetics/metabolism/pathology
MH  - *DNA Methylation
MH  - Humans
MH  - Hyperhomocysteinemia/complications
MH  - Myocytes, Smooth Muscle/pathology
MH  - Oxidative Stress/genetics
OTO - NOTNLM
OT  - DNA methylation
OT  - atherosclerosis
OT  - hyperhomocysteinemia
OT  - inflammation
OT  - oxidative stress
EDAT- 2019/05/23 06:00
MHDA- 2019/11/05 06:00
CRDT- 2019/05/23 06:00
PHST- 2019/05/23 06:00 [entrez]
PHST- 2019/05/23 06:00 [pubmed]
PHST- 2019/11/05 06:00 [medline]
AID - 10.1080/21691401.2019.1617724 [doi]
PST - ppublish
SO  - Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):2031-2041. doi: 
      10.1080/21691401.2019.1617724.