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.
Keywords: Hypoxia, pulmonary hypertension, sheep, fetal programming, newborns.
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