DNA Methylation, Smooth Muscle Cells, and Atherogenesis

Author:

Hiltunen Mikko O.1,Ylä-Herttuala Seppo1

Affiliation:

1. From the A.I. Virtanen Institute (M.O.H., S.Y.-H.) and Department of Medicine (S.Y.-H.), University of Kuopio, and Gene Therapy Unit (S.Y.-H.), Kuopio University Hospital, Kuopio, Finland.

Abstract

DNA methylation is a form of epigenetic modification of the genome that can regulate gene expression. Hypermethylation of CpG islands in the promoter areas leads to decreased gene expression, whereas promoters of actively transcribed genes remain nonmethylated. Because of cellular proliferation and monoclonality of at least some of the lesion cells, atherosclerotic lesions have been compared with benign vascular tumors. 1,2 However, although genetic and epigenetic background favors neoplastic transformation, atherosclerotic plaques never develop to malignant tumors. Among cancer cells, common features are genome-wide hypomethylation, which correlates with transformation and tumor progression. Recent studies have shown that DNA methylation changes occur also during atherogenesis and may contribute to the lesion development.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

Reference43 articles.

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4. Haust MD. The natural history of human atherosclerotic lesions. In: Moore S ed. Vascular Injury and Atherosclerosis. New York: Dekker; 1981: 1–23.

5. Smooth muscle phenotypic modulation: Role in atherogenesis

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