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O2-regulated gene expression: transcriptional control of cardiorespiratory physiology by HIF-1 Semenza GLJ Appl Physiol (1985) 2004[Mar]; 96 (3): 1173-7; discussion 1170-2The cardiovascular and respiratory systems play key roles in O(2) homeostasis. Physiological responses to hypoxia involve changes in gene expression that are mediated by the transcriptional activator hypoxia-inducible factor (HIF)-1. Analysis of mice heterozygous for a knockout allele at the locus encoding the O(2)-regulated HIF-1alpha or HIF-2alpha subunit has revealed that these proteins are required for multiple physiological responses to chronic hypoxia, including erythrocytosis and pulmonary vascular remodeling. In mice with partial HIF-2alpha deficiency, hypoxia-induced expression of endothelin-1 and norepinephrine is dramatically impaired, and the mice fail to develop pulmonary hypertension after 4 wk of exposure to 10% O(2). In mice with partial HIF-1alpha deficiency, the ability of the carotid body to sense and/or respond to acute or chronic hypoxia is lost. In wild-type mice, brief episodes of intermittent hypoxia are sufficient to induce production of erythropoietin (EPO), which protects the heart against apoptosis after ischemia-reperfusion, whereas in mice with partial HIF-1alpha deficiency, intermittent hypoxia does not induce EPO production or cardiac protection. Parenteral administration of EPO to rodents is sufficient to induce dramatic protection against ischemia-reperfusion injury in the heart. Thus HIF-1 mediates critical physiological responses to hypoxia, and the elucidation of these homeostatic mechanisms may lead to novel therapies for the most common causes of mortality in the US population.|*Transcription Factors[MESH]|Animals[MESH]|Cardiovascular System/*metabolism[MESH]|DNA-Binding Proteins/*biosynthesis/genetics[MESH]|Gene Expression Regulation/physiology[MESH]|Humans[MESH]|Hypoxia-Inducible Factor 1[MESH]|Hypoxia-Inducible Factor 1, alpha Subunit[MESH]|Nuclear Proteins/*biosynthesis/genetics[MESH]|Oxygen/*metabolism[MESH]|Respiratory System/*metabolism[MESH]|Transcription, Genetic/*physiology[MESH] |