Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017:2017:1670815.
doi: 10.1155/2017/1670815. Epub 2017 Nov 16.

DNA Methylation and the Potential Role of Methyl-Containing Nutrients in Cardiovascular Diseases

Affiliations
Review

DNA Methylation and the Potential Role of Methyl-Containing Nutrients in Cardiovascular Diseases

Gang Liu et al. Oxid Med Cell Longev. 2017.

Abstract

Patients suffering from cardiovascular diseases (CVDs) experience a low quality of life and increase pressure on healthcare systems both nationally and globally. DNA methylation, which refers to the pathway by which DNA methyltransferase facilitates the addition of a methyl group to DNA, is of critical importance in this respect primarily because the epigenetic modification is implicated in a range of serious conditions including atherosclerosis, CVDs, and cancer. Research findings indicate that the number of epigenetic alterations can be elicited (both in utero and in adults) through the administration of certain nutritional supplements, including folic acid and methionine; this is partly attributable to the effect employed by methyl-containing nutrients in DNA methylation. Thus, for the purpose of illuminating viable therapeutic measures and preventive strategies for CVDs, research should continue to explore the intricate associations that exist between epigenetic regulation and CVD pathogenesis. This review centers on an exposition of the mechanism by which DNA methylation takes place, the impact it has on a range of conditions, and the potential clinical value of nutrition, driven mainly by the observation that nutritional supplements such as folic acid can affect DNA methylation.

PubMed Disclaimer

References

    1. Zhu S., Goldschmidt-Clermont P. J., Dong C. Inactivation of monocarboxylate transporter MCT3 by DNA methylation in atherosclerosis. Circulation. 2005;112(9):1353–1361. doi: 10.1161/CIRCULATIONAHA.104.519025. - DOI - PubMed
    1. Chistiakov D. A., Myasoedova V. A., Orekhov A. N., Bobryshev Y. V. Epigenetically active drugs inhibiting DNA methylation and histone deacetylation. Current Pharmaceutical Design. 2016;22(37):5738–5751. doi: 10.2174/1381612822666160719110618. - DOI - PubMed
    1. Relton C. L., Davey Smith G. Two-step epigenetic Mendelian randomization: a strategy for establishing the causal role of epigenetic processes in pathways to disease. International Journal of Epidemiology. 2012;41(1):161–176. doi: 10.1093/ije/dyr233. - DOI - PMC - PubMed
    1. Sierra M., Valdes A., Fernandez A. F., Torrecillas R., Fraga M. F. The effect of exposure to nanoparticles and nanomaterials on the mammalian epigenome. International Journal of Nanomedicine. 2016;11:6297–6306. doi: 10.2147/IJN.S120104. - DOI - PMC - PubMed
    1. Bernstein B. E., Meissner A., Lander E. S. The mammalian epigenome. Cell. 2007;128(4):669–681. doi: 10.1016/j.cell.2007.01.033. - DOI - PubMed

LinkOut - more resources