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Lock MC, Tellam RL, Botting KJ, et al. The role of miRNA regulation in fetal cardiomyocytes, cardiac maturation and the risk of heart disease in adults. J Physiol. 2018;596(23):5625-5640doi: 10.1113/JP276072.
Lock, M. C., Tellam, R. L., Botting, K. J., Wang, K. C. W., Selvanayagam, J. B., Brooks, D. A., Seed, M., & Morrison, J. L. (2018). The role of miRNA regulation in fetal cardiomyocytes, cardiac maturation and the risk of heart disease in adults. The Journal of physiology, 596(23), 5625-5640. https://doi.org/10.1113/JP276072
Lock, Mitchell C, et al. "The role of miRNA regulation in fetal cardiomyocytes, cardiac maturation and the risk of heart disease in adults." The Journal of physiology vol. 596,23 (2018): 5625-5640. doi: https://doi.org/10.1113/JP276072
Lock MC, Tellam RL, Botting KJ, Wang KCW, Selvanayagam JB, Brooks DA, Seed M, Morrison JL. The role of miRNA regulation in fetal cardiomyocytes, cardiac maturation and the risk of heart disease in adults. J Physiol. 2018 Dec;596(23):5625-5640. doi: 10.1113/JP276072. Epub 2018 Jun 28. PMID: 29785790; PMCID: PMC6265572.
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J Physiol. 2018 Dec;596(23):5625-5640. doi: 10.1113/JP276072. Epub 2018 Jun 28.

The role of miRNA regulation in fetal cardiomyocytes, cardiac maturation and the risk of heart disease in adults.

The Journal of physiology

Mitchell C Lock, Ross L Tellam, Kimberley J Botting, Kimberley C W Wang, Joseph B Selvanayagam, Doug A Brooks, Mike Seed, Janna L Morrison

Affiliations

  1. Early Origins of Adult Health Research Group, School of Pharmacy & Medical Sciences, University of South Australia, Adelaide, SA 5001, Australia.
  2. School of Human Sciences, University of Western Australia, Crawley, WA 6009, Australia.
  3. Cardiac Imaging Research Group, Department of Heart Health, South Australian Health & Medical Research Institute, and Flinders University, GPO Box 2100, Adelaide, SA 5001, Australia.
  4. Mechanisms in Cell Biology and Disease Research Group, School of Pharmacy & Medical Sciences, University of South Australia, Adelaide, SA 5001, Australia.
  5. Hospital for Sick Children, Division of Cardiology, 555 University Avenue, Toronto, ON M5G 1X8, Canada.

PMID: 29785790 PMCID: PMC6265572 DOI: 10.1113/JP276072

Abstract

Myocardial infarction is a primary contributor towards the global burden of cardiovascular disease. Rather than repairing the existing damage of myocardial infarction, current treatments only address the symptoms of the disease and reducing the risk of a secondary infarction. Cardiac regenerative capacity is dependent on cardiomyocyte proliferation, which concludes soon after birth in humans and precocial species such as sheep. Human fetal cardiac tissue has some ability to repair following tissue damage, whereas a fully matured human heart has minimal capacity for cellular regeneration. This is in contrast to neonatal mice and adult zebrafish hearts, which retain the ability to undergo cardiomyocyte proliferation and can regenerate cardiac tissue after birth. In mice and zebrafish models, microRNAs (miRNAs) have been implicated in the regulation of genes involved in cardiac cell cycle progression and regeneration. However, the significance of miRNA regulation in cardiomyocyte proliferation for humans and other large mammals, where the timing of heart development in relation to birth is similar, remains unclear. miRNAs may be valuable targets for therapies that promote cardiac repair after injury. Therefore, elucidating the role of specific miRNAs in large animals, where heart development closely resembles that of humans, remains vitally important for identifying therapeutic targets that may be translated into clinical practice focused on tissue repair.

© 2018 The Authors. The Journal of Physiology © 2018 The Physiological Society.

Keywords: epigenetics; fetal development; heart attack; heart disease; miRNA; programming; regeneration

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