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Epigenetics and Peripheral Artery Disease

  • Genetics (A. Marian, Section Editor)
  • Published:
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Abstract

The term epigenetics is usually used to describe inheritable changes in gene function which do not involve changes in the DNA sequence. These typically include non-coding RNAs, DNA methylation and histone modifications. Smoking and older age are recognised risk factors for peripheral artery diseases, such as occlusive lower limb artery disease and abdominal aortic aneurysm, and have been implicated in promoting epigenetic changes. This brief review describes studies that have associated epigenetic factors with peripheral artery diseases and investigations which have examined the effect of epigenetic modifications on the outcome of peripheral artery diseases in mouse models. Investigations have largely focused on microRNAs and have identified a number of circulating microRNAs associated with human peripheral artery diseases. Upregulating or antagonising a number of microRNAs has also been reported to limit aortic aneurysm development and hind limb ischemia in mouse models. The importance of DNA methylation and histone modifications in peripheral artery disease has been relatively little studied. Whether circulating microRNAs can be used to assist identification of patients with peripheral artery diseases and be modified in order to improve the outcome of peripheral artery disease will require further investigation.

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Correspondence to Jonathan Golledge.

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Conflict of Interest

Jonathan Golledge declares that he works for James Cook University & The Townsville Hospital and declares grant money to his institution from NHMRC, Queensland Government.

Erik Biros, John Bingley, Vikram Iyer, and Smriti M Krishna declare that they have no conflict of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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This article is part of the Topical Collection on Genetics

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Golledge, J., Biros, E., Bingley, J. et al. Epigenetics and Peripheral Artery Disease. Curr Atheroscler Rep 18, 15 (2016). https://doi.org/10.1007/s11883-016-0567-4

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  • DOI: https://doi.org/10.1007/s11883-016-0567-4

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