期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 596, 期 23, 页码 5625-5640出版社
WILEY
DOI: 10.1113/JP276072
关键词
miRNA; epigenetics; heart disease; regeneration; heart attack; fetal development; programming
资金
- NHMRC Career Development Fellowship [APP1066916]
- Australian Research Council Future Fellowship [FT170100431]
- NHMRC Early Career Research Fellowship [APP1090888]
- Australian Government Research Training Program scholarship
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.
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