Impact of epigenetics in the management of cardiovascular disease: a review.
Cardiovascular disease (CVD) is the leading cause of death, irrespective of socioeconomic status, ethnic background and sex. Despite the considerable progress in the treatment, the complex pathophysiology underlying CVD is still not clear. In past few years, genetic approaches including epigenetics and personalized medicine initiated a new way of treating CVD. Epigenetics refers to the non-DNA sequence related heritable changes in gene expression and its role in understanding and treating coronary artery disease, heart failure, and cardiac hypertrophy is currently recognized as an important player. Histone acetylation, deactylation, DNA methylation and histone methylation are different mechanisms of epigenetic modifications. Cardiac Hypertrophy is linked with histone acetylation and the activity of histone acetyltransferases (HATs) has a positive role in cardiac hypertrophy. Altered DNA methylation, miRNA activity have been shown to be associated with atherosclerosis. It is documented that re-expression of certain fetal genes in the adult heart contributes to the development of heart failure syndrome, which is often associated with pathological cardiac remodeling comprising of changes in heart mass, size and shape. Thus, it appears that approaches that counteract epigenetic changes occurring in CVD can prove to have significant therapeutic impact. However, there are no major clinical practice or therapeutics reports of epigenetics contribution in CVD, even though deacetylase inhibitors like trichostatin A were shown to have some positive effects. In this review we will present an overview of various epigenetic mechanisms such as DNA methylation, histone modifications, and microRNA-dependent mechanisms in CVD and the novel epigenetics-based therapeutic approaches.
Graduate School, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China. mwlj521@163.com.
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Cao
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Lu
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Liu
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Li
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Sun
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Zheng
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Zhang
D000818:Animals; D002318:Cardiovascular Diseases / Q000235:genetics* / Q000378:metabolism / Q000628:therapy*; D019175:DNA Methylation / Q000502:physiology; D019468:Disease Management; D044127:Epigenesis, Genetic / Q000502:physiology*; D005786:Gene Expression Regulation; D006321:Heart / Q000502:physiology; D006801:Humans; D035683:MicroRNAs / Q000096:biosynthesis / Q000235:genetics
D035683:MicroRNAs