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Respir Physiol Neurobiol. 2008 Dec 10;164(1-2):282-7. doi: 10.1016/j.resp.2008.07.017.

HIF-1 and ventilatory acclimatization to chronic hypoxia.

Author information

1
Department of Medicine and White Mountain Research Station, University of California, San Diego, La Jolla, CA 92093-0623, USA. fpowell@ucsd.edu

Abstract

Ventilatory acclimatization to hypoxia (VAH) is a time-dependent increase in ventilation and ventilatory O2-sensitivity that involves plasticity in carotid body chemoreceptors and CNS respiratory centers. Hypoxia inducible factor-1alpha (HIF-1alpha) controls the expression of several genes that increase physiological O2 supply. Studies using transgenic mice show HIF-1alpha expression in the carotid bodies and CNS with chronic sustained and intermittent hypoxia is important for VAH. Other O2-sensitive transcription factors such as HIF-2alpha may be important for VAH by reducing metabolic O2 demands also. Specific gene targets of HIF-1alpha shown to be involved in VAH include erythropoietin, endothelin-1, neuronal nitric oxide synthase and tyrosine hydroxylase. Other HIF-1alpha targets that may be involved in VAH include vascular endothelial growth factor, heme oxygenase 1 and cytoglobin. Interactions between these multiple pathways and feedback control of HIF-1alpha expression from some of the targets support a complex and powerful role for HIF-1alpha in neural plasticity of physiological control circuits with chronic hypoxia.

PMID:
18708172
PMCID:
PMC2700119
DOI:
10.1016/j.resp.2008.07.017
[Indexed for MEDLINE]
Free PMC Article

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