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Beyond the genomic paradigm: epigenetic modifications in cardiovascular pathobiology

ESC Congress Report

  • Nutrition alters the epigenetic profile and maternal behaviour influences epigenetic programming
  • Histone and DNA modifications differently dictate gene expression or suppression
  • Long non-coding RNA plays a major role during the transition between embryo and adult rather than during cardiac hypertrophy
  • Methylation pattern differs between healthy and end-stage cardiomyopathic hearts
Basic Sciences, Pharmacology, Genomics and Cardiovascular Pathology


View the Slides from this session in ESC Congress 365

This session reviewed the impact of epigenetic regulation of gene transcription by chromatin remodelling factors (mainly non-coding RNA-based mechanisms, histone modifications and DNA-methylation) on the cardiovascular system and provides insights as to the factors that may influence the epigenome.

First, Jean Louis Gueant reported on how nutrition (e.g., vitamin B, diet enriched in methyl donors) influence the epigenetic mechanisms for gene expression and emphasized the effect of maternal nutrition on the fetal epigenome and its impact on post-natal health.

The impact of different epigenetic writers and erasers (enzymes that alter histones and/or DNA by adding or removing chemical groups, respectively) on cardiac hypertrophy was further examined by Cinzia Perrino, who provided experimental data that shed light on the mechanisms involved.

Gerald W Dorn II provided data to support that long non-coding RNA (lncRNA) are tissue-specific by analyzing heart, liver and skin. Further assessment of lncRNA by heat maps profiling demonstrated that lncRNA-based epigenetic regulation is greater during embryo-adult transition than during reactive hypertrophy. In this regard, Prof. Dorn outlined the involvement of lncRNA in cardiovascular lineage commitment.

In the last talk, Roger Foo presented the genomic response (either protective and/or deleterious) triggered by heart failure and stressed the differential DNA methylation pattern in end-stage human cardiomyopathic hearts as compared to healthy hearts. Dr. Foo pointed out that such different profiling correlated to changes in specific gene expression. Finally, Prof. R. Foo presented transcriptomic analysis that demonstrate that single cell transcriptome signature differ among cells despite being from the same type. 

In summary, the following session provided a comprehensive overview of the available experimental and clinical data on the impact of epigenetics in heart failure and how environmental factors (nutrition) modulates the epigenetic pattern already in early-life playing a role in cardiovascular risk.

References


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SessionTitle:

Beyond the genomic paradigm: epigenetic modifications in cardiovascular pathobiology

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.