FETAL PROGRAMMING AND VASCULAR DYSFUNCTION

DOI

10.1016/j.artres.2017.10.005How to use a DOI?

Keywords

Cardiovascular risk; vascular dysfunction; epigenetic; fetal programming; preeclampsia; ART

Abstract

Cardiovascular diseases are the main cause of mortality and morbidity in Western countries, but the underlying mechanisms are still poorly understood. Genetic polymorphisms, once thought to represent a major determinant of cardiovascular risk, individually and collectively, only explain a tiny fraction of phenotypic variation and disease risk in humans. It is now clear that non-genetic factors, i.e., factors that modify gene activity without changing the DNA sequence and that are sensitive to the environment can cause important alterations of the cardiovascular phenotype in experimental animal models and humans. Here, we will review recent studies demonstrating that distinct pathological events during the perinatal (transient perinatal hypoxemia), late foetal (preeclampsia), and early embryonic (assisted reproductive technologies) periods induce profound alterations of the cardiovascular phenotype in humans and experimental animals. Moreover, we will provide evidence that epigenetic modifications are contributing importantly to this problem and are conferring the potential for its transmission to subsequent generations.

Open Access

This is an open access article distributed under the CC BY-NC license.

TY  - JOUR
AU  - T.A. Meister
AU  - E. Rexhaj
AU  - S.F. Rimoldi
AU  - U. Scherrer
AU  - C. Sartori*
PY  - 2017
DA  - 2017/12/06
TI  - FETAL PROGRAMMING AND VASCULAR DYSFUNCTION
JO  - Artery Research
SP  - 45
EP  - 45
VL  - 20
IS  - C
SN  - 1876-4401
UR  - https://doi.org/10.1016/j.artres.2017.10.005
DO  - 10.1016/j.artres.2017.10.005
ID  - Meister2017
ER  -