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Editorial
The genetics of epigenetics: is there a link with cardiovascular disease
  1. Qingzhong Xiao,
  2. Shu Ye
  1. Centre for Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK
  1. Correspondence to Professor Shu Ye, Centre for Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK; s.ye{at}qmul.ac.uk

https://doi.org/10.1136/hrt.2010.214833

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    There is evidence indicating that altered epigenetic regulation of gene expression in inflammatory and vascular cells plays a role in the development of atherosclerosis and cardiovascular diseases.1 DNA in the nuclei of eukaryotic cells wraps around histone proteins, forming nucleosomes which are further packaged to form chromosomes, and the combination of DNA, histone and other proteins in chromosomes is referred to as the chromatin. Histones are susceptible to chemical modifications which can alter the chromatin structure, consequently increasing or decreasing the accessibility of DNA elements to transcription factors that regulate gene transcription.

    The most extensively studied histone modification is acetylation by the action of histone acetyltransferases.2 P300/CBP-associated factor (PCAF) is one of a number of proteins with acetyltransferase activity and can acetylate histones as well as many non-histone proteins that regulate the expression of genes involved in inflammation and cell proliferation.3–6 In this issue of Heart, Pons et al (see page 143) provide evidence of an association …

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    Footnotes

    • Linked articles 199927.

    • Funding Work in the laboratory of the authors is supported by the British Heart Foundation and forms part of the research themes contributing to the translational research portfolio of Barts and the London Cardiovascular Biomedical Research Unit which is supported and funded by the National Institute of Health Research. QX is the recipient of a British Heart Foundation Intermediate Basic Science Research Fellowship (FS/09/044/28007).

    • Competing interests None.

    • Provenance and peer review Commissioned; not externally peer reviewed.

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