TY - JOUR
T1 - Intrauterine growth restriction - Etiology and consequences
T2 - What do we know about the human situation and experimental animal models?
AU - Ergaz, Zivanit
AU - Avgil, Meytal
AU - Ornoy, Asher
PY - 2005/9
Y1 - 2005/9
N2 - Embryonic and fetal growth depend on genetic and environmental factors, and the process is the result of the interaction between these factors. About 7-9% of live-born infants have a birth weight below normal (below the 10th percentile). The rate and extent of intrauterine growth restriction (IUGR) varies by ethnicity and socio-economic status. Some of the suspected causes of IUGR are as follows. (1) Maternal factors such as inadequate or severe malnutrition, chronic maternal diseases, birth order, multiple births, and parental genetic factors. (2) Placental pathology, mainly placental vascular damage that may lead to placental insufficiency. This is often found in maternal diseases such as pre-eclampsia, and Thrombophilia. (3) Intrauterine infections and specific fetal syndromes, including chromosomal aberrations. (4) Non-classified causes such as adolescent's pregnancy, maternal smoking and alcohol drinking, living at high altitudes. Several existing animal models for IUGR, including uterine artery ligation or gene knock out models, although insightful of potential mechanism(s) underlying intrauterine growth restriction, are limited in that they do not reflect human causality. As the ultimate goal is prevention, we seem still to be distant from achieving this goal.
AB - Embryonic and fetal growth depend on genetic and environmental factors, and the process is the result of the interaction between these factors. About 7-9% of live-born infants have a birth weight below normal (below the 10th percentile). The rate and extent of intrauterine growth restriction (IUGR) varies by ethnicity and socio-economic status. Some of the suspected causes of IUGR are as follows. (1) Maternal factors such as inadequate or severe malnutrition, chronic maternal diseases, birth order, multiple births, and parental genetic factors. (2) Placental pathology, mainly placental vascular damage that may lead to placental insufficiency. This is often found in maternal diseases such as pre-eclampsia, and Thrombophilia. (3) Intrauterine infections and specific fetal syndromes, including chromosomal aberrations. (4) Non-classified causes such as adolescent's pregnancy, maternal smoking and alcohol drinking, living at high altitudes. Several existing animal models for IUGR, including uterine artery ligation or gene knock out models, although insightful of potential mechanism(s) underlying intrauterine growth restriction, are limited in that they do not reflect human causality. As the ultimate goal is prevention, we seem still to be distant from achieving this goal.
KW - Animal models
KW - Etiology
KW - Human
KW - IUGR
KW - SGA
UR - http://www.scopus.com/inward/record.url?scp=21744432840&partnerID=8YFLogxK
U2 - 10.1016/j.reprotox.2005.04.007
DO - 10.1016/j.reprotox.2005.04.007
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C2 - 15982850
AN - SCOPUS:21744432840
SN - 0890-6238
VL - 20
SP - 301
EP - 322
JO - Reproductive Toxicology
JF - Reproductive Toxicology
IS - 3
ER -