Molecular mechanisms underlying the fetal programming of adult disease

被引:37
作者
Vo, Thin [1 ,2 ,3 ,4 ]
Hardy, Daniel B. [1 ,2 ,3 ,4 ]
机构
[1] Univ Western Ontario, Dept Physiol & Pharmacol, London, ON N6A 5C1, Canada
[2] Univ Western Ontario, Dept Obstet & Gynecol, London, ON N6A 5C1, Canada
[3] Childrens Hlth Res Inst, London, ON N6C 2V5, Canada
[4] Lawson Hlth Res Inst, London, ON N6A 4V2, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
Fetal Programming; Epigenetics; microRNA; Posttranslational Histone Modifications; DNA Methylation; ER Stress; Nuclear Receptors; ENDOPLASMIC-RETICULUM STRESS; ACTIVATED-RECEPTOR-GAMMA; LOW-PROTEIN DIET; INTRAUTERINE GROWTH RESTRICTION; HEPATIC PHOSPHOENOLPYRUVATE CARBOXYKINASE; FOLIC-ACID SUPPLEMENTATION; SYSTOLIC BLOOD-PRESSURE; ISCHEMIC-HEART-DISEASE; ENZYME GENE-EXPRESSION; GLUCOCORTICOID-RECEPTOR;
D O I
10.1007/s12079-012-0165-3
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
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
收藏
页码:139 / 153
页数:15
相关论文
共 169 条
[1]   Maternal dietary protein restriction and excess affects offspring gene expression and methylation of non-SMC subunits of condensin I in liver and skeletal muscle [J].
Altmann, Simone ;
Murani, Eduard ;
Schwerin, Manfred ;
Metges, Cornelia C. ;
Wimmers, Klaus ;
Ponsuksili, Siriluck .
EPIGENETICS, 2012, 7 (03) :239-252
[2]   PPARδ regulates satellite cell proliferation and skeletal muscle regeneration [J].
Angione, Alison R. ;
Jiang, Chunhui ;
Pan, Dongning ;
Wang, Yong-Xu ;
Kuang, Shihuan .
SKELETAL MUSCLE, 2011, 1
[3]   A NOVEL ORPHAN RECEPTOR-SPECIFIC FOR A SUBSET OF THYROID HORMONE-RESPONSIVE ELEMENTS AND ITS INTERACTION WITH THE RETINOID/THYROID HORMONE-RECEPTOR SUBFAMILY [J].
APFEL, R ;
BENBROOK, D ;
LERNHARDT, E ;
ORTIZ, MA ;
SALBERT, G ;
PFAHL, M .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (10) :7025-7035
[4]   Effects of peroxisome proliferator-activated receptor δ on placentation, adiposity, and colorectal cancer [J].
Barak, Y ;
Liao, D ;
He, WM ;
Ong, ES ;
Nelson, MC ;
Olefsky, JM ;
Boland, R ;
Evans, RM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (01) :303-308
[5]   THE FETAL AND INFANT ORIGINS OF ADULT DISEASE [J].
BARKER, DJP .
BRITISH MEDICAL JOURNAL, 1990, 301 (6761) :1111-1111
[6]   Fetal origins of adult disease:: strength of effects and biological basis [J].
Barker, DJP ;
Eriksson, JG ;
Forsén, T ;
Osmond, C .
INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, 2002, 31 (06) :1235-1239
[7]   Anti-inflammatory actions of glucocorticoids: molecular mechanisms [J].
Barnes, PJ .
CLINICAL SCIENCE, 1998, 94 (06) :557-572
[8]   Fast signals and slow marks: the dynamics of histone modifications [J].
Barth, Teresa K. ;
Imhof, Axel .
TRENDS IN BIOCHEMICAL SCIENCES, 2010, 35 (11) :618-626
[9]   Developmental plasticity and human health [J].
Bateson, P ;
Barker, D ;
Clutton-Brock, T ;
Deb, D ;
D'Udine, B ;
Foley, RA ;
Gluckman, P ;
Godfrey, K ;
Kirkwood, T ;
Lahr, MM ;
McNamara, J ;
Metcalfe, NB ;
Monaghan, P ;
Spencer, HG ;
Sultan, SE .
NATURE, 2004, 430 (6998) :419-421
[10]   A maternal cafeteria diet during gestation and lactation promotes adiposity and impairs skeletal muscle development and metabolism in rat offspring at weaning [J].
Bayol, SA ;
Simbi, BH ;
Stickland, NC .
JOURNAL OF PHYSIOLOGY-LONDON, 2005, 567 (03) :951-961