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Maternal smoking as a model for environmental epigenetic changes affecting birthweight and fetal programming
Author(s) -
Melissa Suter,
Amber Anders,
Kjersti M. Aagaard
Publication year - 2012
Publication title -
molecular human reproduction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.143
H-Index - 122
eISSN - 1460-2407
pISSN - 1360-9947
DOI - 10.1093/molehr/gas050
Subject(s) - in utero , epigenome , fetus , biology , epigenetics , fetal programming , pregnancy , tobacco smoke , nicotine , physiology , fetal growth , dna methylation , genetics , medicine , environmental health , gene expression , neuroscience , gene
Although the association between maternal smoking and low birthweight infants has been well established, the mechanisms behind reduced fetal growth are still being elucidated. While many infants are exposed to tobacco smoke in utero, not all are born growth restricted or small for gestational age. Many hypotheses have emerged to explain the differential response to in utero maternal tobacco smoke exposure (MTSE). Studies have shown that both maternal and fetal genotypes may contribute to the discrepant outcomes. However, the contribution of epigenetic changes cannot be ignored. In this review we address two important questions regarding the effect of MTSE on the fetal epigenome. First, does exposure to maternal tobacco smoke in utero alter the fetal epigenome? Secondly, could these alterations be associated with the reduced fetal growth observed with MTSE?

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