Maternal transmission of risk for atherosclerosis.
OBJECTIVE
In the last 20 years, an increasing amount of epidemiological and pathological evidence has become available illustrating the relationship between an adverse in-utero environment and increased risk of vascular disease in the offspring. It is now generally accepted that epigenetic phenomena, such as either DNA methylation or chromatin modifications or both mediate the long-term memory and thus developmental programming of cells and tissues.


RESULTS
In utero, the placenta and fetus are exposed to the metabolic, antioxidant and pro-inflammatory and anti-inflammatory signals from the mother and will likely respond specifically. In the fetus, these responses may lead to permanent changes either in DNA methylation or chromatin modification or both and these changes may lead to increased atherosclerosis susceptibility in adulthood. However, the molecular mechanisms responsible for the translation of an adverse maternal environment into permanent epigenetic changes are poorly understood.


CONCLUSIONS
In this review, we briefly summarize the possible signals crossing the placental barrier and discuss the molecular mechanisms of epigenetic programming in the developing fetus leading to increased athero-susceptibility of the vessel wall.
DeRuiter
Marco C
MC
Department of Anatomy and Embryology, Leiden University Medical Center, Leiden, The Netherlands. m.c.deruiter@lumc.nl
Alkemade
Fanneke E
FE
Gittenberger-de Groot
Adriana C
AC
Poelmann
Robert E
RE
Havekes
Louis M
LM
van Dijk
Ko Willems
KW
D000818:Animals; D050197:Atherosclerosis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D005333:Fetus / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006937:Hypercholesterolemia / Q000378:metabolism / Q000473:pathology; D044342:Malnutrition / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000503:physiopathology*; D012306:Risk