期刊
CURRENT VASCULAR PHARMACOLOGY
卷 11, 期 5, 页码 616-640出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1570161111311050006
关键词
Hypoxia; pulmonary hypertension; sheep; fetal programming; newborns
资金
- National Science Foundation under Major Research Instrumentation, Division of Biological Infrastructure Grant [0923559]
- Loma Linda University School of Medicine
- USPHS [HD069746, HL095973, HD/HL-03807, HD-31226]
- Div Of Biological Infrastructure
- Direct For Biological Sciences [923559] Funding Source: National Science Foundation
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.
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