Fetal programming and vascular dysfunction

T.A. Meister; E. Rexhaj; S.F. Rimoldi; U. Scherrer; C. Sartori

doi:10.1016/j.artres.2017.11.005

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Volume 21, Issue C, March 2018, Pages 69 - 77

Fetal programming and vascular dysfunction

Authors

T.A. Meister^a, E. Rexhaj^a, S.F. Rimoldi^a, U. Scherrer^a^{, b}, C. Sartori^c^{, *}

^aDepartments of Cardiology and Clinical Research, University Hospital Bern, 3010 Bern, Switzerland

^bFacultad de Ciencias, Departamento de Biología, Universidad de Tarapacá, 1775 Arica, Chile

^cInternal Medicine, University Hospital, 1011 Lausanne-CHUV, Switzerland

^*Corresponding author. Internal Medicine, University Hospital, 1011 Lausanne-CHUV, Switzerland. E-mail address: Claudio.Sartori@chuv.ch (C. Sartori).

Corresponding Author

C. Sartori

Available Online 13 December 2017.

DOI: 10.1016/j.artres.2017.11.005 How 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.

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Journal: Artery Research
Volume-Issue: 21 - C
Pages: 69 - 77
Publication Date: 2017/12/13
ISSN (Online): 1876-4401
ISSN (Print): 1872-9312
DOI: 10.1016/j.artres.2017.11.005 How to use a DOI?
Open Access: This is an open access article distributed under the CC BY-NC license.

Cite this article

ris enw bib

TY  - JOUR
AU  - T.A. Meister
AU  - E. Rexhaj
AU  - S.F. Rimoldi
AU  - U. Scherrer
AU  - C. Sartori
PY  - 2017
DA  - 2017/12/13
TI  - Fetal programming and vascular dysfunction
JO  - Artery Research
SP  - 69
EP  - 77
VL  - 21
IS  - C
SN  - 1876-4401
UR  - https://doi.org/10.1016/j.artres.2017.11.005
DO  - 10.1016/j.artres.2017.11.005
ID  - Meister2017
ER  -

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