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|Scopus||Web of Science®|
|Title:||Early origins of heart disease: low birth weight and determinants of cardiomyocyte endowment|
|Citation:||Clinical and Experimental Pharmacology and Physiology, 2012; 39(9):814-823|
|Publisher:||Blackwell Publishing Asia|
|K.J. Botting, K.C.W. Wang, M. Padhee, I.C. McMillen, B. Summers-Pearce, L. Rattanatray, N. Cutri, G.S. Posterino, D.A. Brooks and J.L. Morrison|
|Abstract:||SUMMARY: 1. World-wide epidemiological and experimental animal studies demonstrate that adversity in fetal life, resulting in intrauterine growth restriction, programmes the offspring for a greater susceptibility to ischaemic heart disease and heart failure in adult life. 2. After cardiogenesis, cardiomyocyte endowment is determined by a range of hormones and signalling pathways that regulate cardiomyocyte proliferation, apoptosis and the timing of multinucleation terminal differentiation. 3. The small fetus may have reduced cardiomyocyte endowment owing to the impact of a suboptimal intrauterine environment on the signalling pathways that regulate cardiomyocyte proliferation, apoptosis and the timing of terminal differentiation.|
|Keywords:||Apoptosis; cardiomyocyte endowment; intrauterine growth restriction; multinucleation; proliferation|
|Rights:||© 2012 The Authors Clinical and Experimental Pharmacology and Physiology © 2012 Wiley Publishing Asia Pty Ltd.|
|Appears in Collections:||Medical Sciences publications|
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