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Breath of Life: Heart Disease Link to Developmental Hypoxia.

Published version
Peer-reviewed

Type

Article

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Authors

Abstract

Heart disease remains one of the greatest killers. In addition to genetics and traditional lifestyle risk factors, we now understand that adverse conditions during pregnancy can also increase susceptibility to cardiovascular disease in the offspring. Therefore, the mechanisms by which this occurs and possible preventative therapies are of significant contemporary interest to the cardiovascular community. A common suboptimal pregnancy condition is a sustained reduction in fetal oxygenation. Chronic fetal hypoxia results from any pregnancy with increased placental vascular resistance, such as in preeclampsia, placental infection, or maternal obesity. Chronic fetal hypoxia may also arise during pregnancy at high altitude or because of maternal respiratory disease. This article reviews the short- and long-term effects of hypoxia on the fetal cardiovascular system, and the importance of chronic fetal hypoxia in triggering a developmental origin of future heart disease in the adult progeny. The work summarizes evidence derived from human studies as well as from rodent, avian, and ovine models. There is a focus on the discovery of the molecular link between prenatal hypoxia, oxidative stress, and increased cardiovascular risk in adult offspring. Discussion of mitochondria-targeted antioxidant therapy offers potential targets for clinical intervention in human pregnancy complicated by chronic fetal hypoxia.

Description

Keywords

fetus, hypoxia, mitochondria, oxidative stress, Animals, Cell Hypoxia, Female, Heart Diseases, Humans, Male, Oxidative Stress

Journal Title

Circulation

Conference Name

Journal ISSN

0009-7322
1524-4539

Volume Title

144

Publisher

Ovid Technologies (Wolters Kluwer Health)
Sponsorship
British Heart Foundation (None)
MRC (unknown)
British Heart Foundation (None)
British Heart Foundation (RG/17/8/32924)
British Heart Foundation (via University of Manchester) (R122324)
The work is supported by The British Heart Foundation (RG/17/8/32924) and the Medical Research Council UK (MR/V03362X/1).