Is Any Cardiovascular Disease-Specific DNA Methylation Biomarker Within Reach?
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GENETICS AND GENOMICS (A.J. MARIAN, SECTION EDITOR)
Is Any Cardiovascular Disease-Specific DNA Methylation Biomarker Within Reach? Carmen de la Rocha 1 & Silvio Zaina 2 & Gertrud Lund 3
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review A detailed understanding of the epigenome of cardiovascular disease (CVD) should broaden current insights into mechanisms of atherogenesis and help identify suitable biomarkers for disease risk and progression. This review addresses the question whether a consensus has been reached on identifying the main aberrant DNA methylation profile in CVD. Additionally, it presents advances and setbacks in the search for specific CVD biomarkers. Recent Findings Although the literature points to DNA hypermethylation as an epigenetic landmark of CVD, inconsistencies are significant. In particular, the DNA methylomes of peripheral blood cells and the vascular wall do not show a consistent direction of change in all studies. An additional significant hurdle is the relatively low study-to-study reproducibility and the difficulty to assess specificity for CVD. Nonetheless, a number of biologically plausible markers have been proposed that warrant further studies. Summary An integrated model for dynamic changes of DNA methylation during the natural history of atherosclerosis predisposition and progression is presented, that might reconcile conflicting findings. Cohort design and technical criteria for DNA methylation analysis need to be further homogenized to allow for meaningful validation. As stable DNA methylation profiles are likely determined by genetic variants, many of which might control a range of diseases, it is anticipated that CVD biomarker discovery will be a delicate balancing act between reproducibility and specificity. Keywords Atherosclerosis . DNA methylation . Biomarker . Differentially methylated region . Epigenomics
Introduction Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. CVD is responsible for an estimated
This article is part of the Topical Collection on Genetics and Genomics Copyright Figures and tables are original and were created entirely with inputs from each of the authors. * Gertrud Lund [email protected] 1
Department of Molecular Biology and Genomics, University Center for Health Sciences, University of Guadalajara, Guadalajara, Jal., Mexico
2
Department of Medical Sciences, Division of Health Sciences, Leon Campus, University of Guanajuato, Leon, Gto., Mexico
3
Department of Genetic Engineering, CINVESTAV Irapuato Unit, Km. 9.6 Libramiento Norte Carr. Irapuato-León, 36824 Irapuato, Gto., Mexico
~18 million deaths per year or ~ 30% of deaths globally [1]. Atherosclerosis, the dominant pathology leading to CVD, is characterized by lipid accumulation, inflammatory responses, cell proliferation and death, and fibrosis in the arterial wall [2]. The pathogenesis of atherosclerosis initiates with the appearance of fatty streak on the luminal side of arteries leading to for
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