Translational Perspective on Epigenetics in Cardiovascular Disease

Harst, Pim van der; Windt, León J. De; Chambers, John C.

doi:10.1016/j.jacc.2017.05.067

Cited by 86 publications

(46 citation statements)

References 126 publications

(174 reference statements)

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“…(i) DNA methylation is defined by the covalent binding of a methyl group to the 5 carbon of cytosine and is usually associated with gene expression repression, as it can decrease the accessibility of chromatin to DNA-binding proteins or transcription factors that are required for gene transcriptional activation [26].…”

Section: Alterations In Myocardial Compliance and Progression Of Cardmentioning

confidence: 99%

Cell-Based Mechanosensation, Epigenetics, and Non-Coding RNAs in Progression of Cardiac Fibrosis

Ferrari

Pesce

2019

IJMS

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The heart is par excellence the ‘in-motion’ organ in the human body. Compelling evidence shows that, besides generating forces to ensure continuous blood supply (e.g., myocardial contractility) or withstanding passive forces generated by flow (e.g., shear stress on endocardium, myocardial wall strain, and compression strain at the level of cardiac valves), cells resident in the heart respond to mechanical cues with the activation of mechanically dependent molecular pathways. Cardiac stromal cells, most commonly named cardiac fibroblasts, are central in the pathologic evolution of the cardiovascular system. In their normal function, these cells translate mechanical cues into signals that are necessary to renew the tissues, e.g., by continuously rebuilding the extracellular matrix being subjected to mechanical stress. In the presence of tissue insults (e.g., ischemia), inflammatory cues, or modifiable/unmodifiable risk conditions, these mechanical signals may be ‘misinterpreted’ by cardiac fibroblasts, giving rise to pathology programming. In fact, these cells are subject to changing their phenotype from that of matrix renewing to that of matrix scarring cells—the so-called myo-fibroblasts—involved in cardiac fibrosis. The links between alterations in the abilities of cardiac fibroblasts to ‘sense’ mechanical cues and molecular pathology programming are still under investigation. On the other hand, various evidence suggests that cell mechanics may control stromal cells phenotype by modifying the epigenetic landscape, and this involves specific non-coding RNAs. In the present contribution, we will provide examples in support of this more integrated vision of cardiac fibrotic progression based on the decryption of mechanical cues in the context of epigenetic and non-coding RNA biology.

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Section: Alterations In Myocardial Compliance and Progression Of Cardmentioning

confidence: 99%

Cell-Based Mechanosensation, Epigenetics, and Non-Coding RNAs in Progression of Cardiac Fibrosis

Ferrari

Pesce

2019

IJMS

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“…Multiple excellent reviews focus on epigenetics and cardiovascular disease in adults. 9,[19][20][21] These mechanisms similarly apply to pediatric cardiovascular disease, and, in fact, some are unique to pediatric cardiology. Here, we will highlight several mechanisms that relate to pediatric heart disease, including both congenital and acquired heart disease.…”

Section: M P a Ct Of E P I Gen E Ti Cs I N Con Ge N It Al A N D Amentioning

confidence: 99%

“…Gene regulatory ncRNA primarily includes microRNA (miR), long noncoding RNA (lncRNA), small interfering RNA, antisense RNA, and piwi-interacting RNA. 9 MiRs are the best studied group of ncRNAs. For simplicity, this review will focus on miRs.…”

Section: R Na -M Ed I a Te D R E Gu La Ti Onmentioning

confidence: 99%

Epigenetics for the pediatric cardiologist

Spearman

2017

Congenital Heart Disease

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A genetic basis of congenital heart disease (CHD) has been known for decades. In addition to the sequence of the genome, the contribution of epigenetics to pediatric cardiology is increasingly recognized. Multiple epigenetic mechanisms, including DNA methylation, histone modification, and RNA-based regulation, are known mediators of cardiovascular disease, including both development and progression of CHD and its sequelae. Basic understanding of the concepts of epigenetics will be essential to all pediatric cardiologists in order to understand mechanisms of pathophysiology, pharmacotherapeutic concepts, and to understand the role of epigenetics in precision medicine.

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“…Assessing what smoking-associated methylation changes are transient or long-lasting may have important implications for biological understanding and clinical practice. 15…”

Section: Introductionmentioning

confidence: 99%

“…They also observed differential methylation in former smokers who had quit more than 40 years before methylation measurement, compared to never smokers. Assessing what smoking-associated methylation changes are transient or long-lasting may have important implications for biological understanding and clinical practice [14] .…”

Section: Introductionmentioning

confidence: 99%

Smoking and blood DNA methylation: novel associations, replication of previous findings and assessment of reversibility

Dugué

Jung

et al. 2019

Preprint

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We conducted a genome-wide association study of blood DNA methylation and smoking, attempted replication of previously discovered associations, and assessed the reversibility of smokingassociated methylation changes. DNA methylation was measured in baseline peripheral blood samples for 5,044 participants in the Melbourne Collaborative Cohort Study. For 1,032 participants, these measures were repeated using blood samples collected at follow-up, a median of 11 years later.A cross-sectional analysis of the association between smoking and DNA methylation and a

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Translational Perspective on Epigenetics in Cardiovascular Disease

Cited by 86 publications

References 126 publications

Cell-Based Mechanosensation, Epigenetics, and Non-Coding RNAs in Progression of Cardiac Fibrosis

Cell-Based Mechanosensation, Epigenetics, and Non-Coding RNAs in Progression of Cardiac Fibrosis

Epigenetics for the pediatric cardiologist

Smoking and blood DNA methylation: novel associations, replication of previous findings and assessment of reversibility

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