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Epigenetic Regulation of Endothelial-to-Mesenchymal Transition in Chronic Heart Disease: Histone Modifications, DNA Methylation, and Noncoding RNAs

Hulshoff, M. S., Xu, X., Krenning, G. & Zeisberg, E. M., Sep-2018, In : Arteriosclerosis thrombosis and vascular biology. 38, 9, p. 1986-1996 11 p.

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  • Epigenetic Regulation of Endothelial-to-Mesenchymal Transition in Chronic Heart Disease

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DOI

Endothelial-to-mesenchymal transition (EndMT) is a process in which endothelial cells lose their properties and transform into fibroblast-like cells. This transition process contributes to cardiac fibrosis, a common feature of patients with chronic heart failure. To date, no specific therapies to halt or reverse cardiac fibrosis are available, so knowledge of the underlying mechanisms of cardiac fibrosis is urgently needed. In addition, EndMT contributes to other cardiovascular pathologies such as atherosclerosis and pulmonary hypertension, but also to cancer and organ fibrosis. Remarkably, the molecular mechanisms driving EndMT are largely unknown. Epigenetics play an important role in regulating gene transcription and translation and have been implicated in the EndMT process. Therefore, epigenetics might be the missing link in unraveling the underlying mechanisms of EndMT. Here, we review the involvement of epigenetic regulators during EndMT in the context of cardiac fibrosis. The role of DNA methylation, histone modifications (acetylation and methylation), and noncoding RNAs (microRNAs, long noncoding RNAs, and circular RNAs) in the facilitation and inhibition of EndMT are discussed, and potential therapeutic epigenetic targets will be highlighted.

Original languageEnglish
Pages (from-to)1986-1996
Number of pages11
JournalArteriosclerosis thrombosis and vascular biology
Volume38
Issue number9
Publication statusPublished - Sep-2018

    Keywords

  • acetylation, DNA methylation, endothelial cells, epigenomics, fibrosis, heart failure, RNA, untranslated, INDUCED CARDIAC FIBROSIS, GROWTH-FACTOR-BETA, FLUID SHEAR-STRESS, FIBROBLAST ACTIVATION, HUMAN GENOME, PROMOTER HYPERMETHYLATION, INFLAMMATORY CYTOKINES, PULMONARY-HYPERTENSION, DILATED CARDIOMYOPATHY, CIRCULATING MICRORNAS

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