Antenatal hypoxia and pulmonary vascular function and remodeling.

Abstract:

:This review provides evidence that antenatal hypoxia, which represents a significant and worldwide problem, causes prenatal programming of the lung. A general overview of lung development is provided along with some background regarding transcriptional and signaling systems of the lung. The review illustrates that antenatal hypoxic stress can induce a continuum of responses depending on the species examined. Fetuses and newborns of certain species and specific human populations are well acclimated to antenatal hypoxia. However, antenatal hypoxia causes pulmonary vascular disease in fetuses and newborns of most mammalian species and humans. Disease can range from mild pulmonary hypertension, to severe vascular remodeling and dangerous elevations in pressure. The timing, length, and magnitude of the intrauterine hypoxic stress are important to disease development, however there is also a genetic-environmental relationship that is not yet completely understood. Determining the origins of pulmonary vascular remodeling and pulmonary hypertension and their associated effects is a challenging task, but is necessary in order to develop targeted therapies for pulmonary hypertension in the newborn due to antenatal hypoxia that can both treat the symptoms and curtail or reverse disease progression.

journal_name

Curr Vasc Pharmacol

authors

Papamatheakis DG,Blood AB,Kim JH,Wilson SM

doi

10.2174/1570161111311050006

subject

Has Abstract

pub_date

2013-09-01 00:00:00

pages

616-40

issue

5

eissn

1570-1611

issn

1875-6212

pii

CVP-56292

journal_volume

11

pub_type

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