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Maternal transmission of risk for atherosclerosis

DeRuiter, Marco Ca; Alkemade, Fanneke Ea; Gittenberger-de Groot, Adriana Ca; Poelmann, Robert Ea; Havekes, Louis Mc; van Dijk, Ko Willemsb

doi: 10.1097/MOL.0b013e328304b670
Hyperlipidaemia and cardiovascular disease: Edited by Paul N. Durrington
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Purpose of review 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.

Recent findings 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.

Summary 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.

aDepartment of Anatomy and Embryology, The Netherlands

bDepartment of Human Genetics, Leiden University Medical Center, The Netherlands

cTNO-Quality of Life, Gaubius Laboratory, Leiden, The Netherlands

Correspondence to Dr M.C. DeRuiter, PhD, Department of Anatomy and Embryology, Leiden University Medical Center, PO BOX 9600, 2300 RC Leiden, The Netherlands Tel: +31 71 5269308; fax: +31 71 5268289; e-mail: m.c.deruiter@lumc.nl

© 2008 Lippincott Williams & Wilkins, Inc.