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Early origins of heart disease: Low birth weight and determinants of cardiomyocyte endowment
Author(s) -
Botting KJ,
Wang KCW,
Padhee M,
McMillen IC,
SummersPearce B,
Rattanatray L,
Cutri N,
Posterino GS,
Brooks DA,
Morrison JL
Publication year - 2012
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2011.05649.x
Subject(s) - offspring , biology , intrauterine growth restriction , fetus , heart disease , apoptosis , endocrinology , hormone , heart development , heart failure , endowment , disease , medicine , microbiology and biotechnology , pregnancy , embryonic stem cell , genetics , gene , philosophy , epistemology
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.