Molecular mechanisms underlying the fetal programming of adult disease

被引:0
|
作者
Thin Vo
Daniel B. Hardy
机构
[1] University of Western Ontario,The Department of Physiology & Pharmacology
[2] University of Western Ontario,The Department of Obstetrics & Gynecology
[3] The Children’s Health Research Institute,undefined
[4] The Lawson Health Research Institute,undefined
来源
Journal of Cell Communication and Signaling | 2012年 / 6卷
关键词
Fetal Programming; Epigenetics; microRNA; Posttranslational Histone Modifications; DNA Methylation; ER Stress; Nuclear Receptors;
D O I
暂无
中图分类号
学科分类号
摘要
Adverse events in utero can be critical in determining quality of life and overall health. It is estimated that up to 50 % of metabolic syndrome diseases can be linked to an adverse fetal environment. However, the mechanisms linking impaired fetal development to these adult diseases remain elusive. This review uncovers some of the molecular mechanisms underlying how normal physiology may be impaired in fetal and postnatal life due to maternal insults in pregnancy. By understanding the mechanisms, which include epigenetic, transcriptional, endoplasmic reticulum (ER) stress, and reactive oxygen species (ROS), we also highlight how intervention in fetal and neonatal life may be able to prevent these diseases long-term.
引用
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页码:139 / 153
页数:14
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