Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/74769
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: Early origins of heart disease: low birth weight and the role of the insulin-like growth factor system in cardiac hypertrophy
Author: Wang, K.
Botting, K.
Padhee, M.
Zhang, S.
McMillen, I.
Suter, C.
Brooks, D.
Morrison, J.
Citation: Clinical and Experimental Pharmacology and Physiology, 2012; 39(11):958-964
Publisher: Blackwell Publishing Asia
Issue Date: 2012
ISSN: 0305-1870
1440-1681
Statement of
Responsibility: 
Kimberley CW Wang, Kimberley J Botting, Monalisa Padhee, Song Zhang, I Caroline McMillen, Catherine M Suter, Doug A Brooks and Janna L Morrison
Abstract: Epidemiological studies indicate that poor growth before birth is associated with left ventricular hypertrophy and an increased risk of death from heart disease later in life. In fetal life, the insulin-like growth factor (IGF) system has been implicated in physiological growth of the heart, whereas in postnatal life IGFs can be involved in both physiological and pathological cardiac hypertrophy. A reduction in substrate supply in fetal life, resulting in chronic hypoxaemia and intrauterine growth restriction, results in increased cardiac IGF-1R, IGF-2 and IGF-2R gene expression; and there is also evidence for a role of the IGF-2 receptor in the ensuing cardiac hypertrophy. The persistent high level of cardiac IGF-2R gene expression from fetal to postnatal life may be due to epigenetic changes in key cardiac hypertrophy regulatory pathways.
Keywords: epigenetics
hypertrophy
insulin-like growth factors
intrauterine growth restriction
Rights: © 2012 The Authors Clinical and Experimental Pharmacology and Physiology © 2012 Wiley Publishing Asia Pty Ltd
DOI: 10.1111/j.1440-1681.2012.05743.x
Grant ID: http://purl.org/au-research/grants/nhmrc/349405
Published version: http://dx.doi.org/10.1111/j.1440-1681.2012.05743.x
Appears in Collections:Aurora harvest 4
Pharmacology publications

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.