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Epigenetics and Atherosclerosis

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Abstract

Atherosclerotic risk factors can be divided into two main categories—genetical and environmental issues. The latter ones include habitual factors since human habits manifest as environmental factors at the cellular level. Environmental issues can govern human health via epigenetic modification of chromatin structure. This review discusses the recent findings linking general epigenetic mechanisms of chromatin modifications to atherosclerosis development.

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Abbreviations

ApoE:

Apolipoprotein E

CHD:

Coronary heart disease

CpG:

Cytosine–Guanine dinucleotide

CTCF:

CCCTC-binding factor

ECM:

Extracellular matrix

ERα:

Estrogen receptor alpha

ERβ:

Estrogen receptor beta

FGF2:

Fibroblast growth factor 2

HAT:

Histone acetyl transferase

Hcy:

Homocysteine

HDAC:

Histone deacetylase

HIF1α:

Hypoxia inducible factor 1α

IGF2:

Insulin-like growth factor 2

KAT2B:

Lysine acetyltransferase 2B

LDL:

Low density lipoprotein

LDLR:

LDL receptor

MBD:

Methyl-cytosine-binding protein

NOS:

Nitric oxide synthase

PBL:

Peripheral blood lymphocytes

POL2:

RNA polymerase II

RISC:

RNA induced silencing

SAH:

S-adenosylhomocysteine

SAM:

S-adenosylmethionine

siRNA:

Small interfering RNA

SMC:

Smooth muscle cell

SNP:

Single nucleotide polymorphism

SRF:

Serum response factor

TGS:

Transcriptional gene silencing

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Acknowledgments

This work was supported by Finnish Academy, Leducq Foundation, CliniGene EU grant, and Ark Therapeutics Ltd.

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Aavik, E., Turunen, M.P., Ylä-Herttuala, S. (2012). Epigenetics and Atherosclerosis. In: Minarovits, J., Niller, H. (eds) Patho-Epigenetics of Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-3345-3_13

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