Early Origins of Adult Health Research Group, Sansom Institute for Health Research, School of Pharmacy and Medical Sciences, University of Adelaide, Adelaide, South Australia, Australia.
Clin Exp Pharmacol Physiol. 2012 Nov;39(11):958-64. doi: 10.1111/j.1440-1681.2012.05743.x.
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.
流行病学研究表明，出生前生长不良与左心室肥厚和晚年死于心脏病的风险增加有关。在胎儿期，胰岛素样生长因子 (IGF) 系统与心脏的生理生长有关，而在出生后，IGFs 可参与生理性和病理性心肌肥厚。胎儿期底物供应减少导致慢性低氧血症和宫内生长受限，导致心脏 IGF-1R、IGF-2 和 IGF-2R 基因表达增加；IGF-2 受体在随后的心脏肥厚中也有作用。从胎儿期到出生后，心脏 IGF-2R 基因表达持续高水平可能是由于关键心脏肥厚调节途径中的表观遗传变化。
