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Article: Hypoxia-inducible factor-1: A molecular hint of physiological changes in the carotid body during long-term hypoxemia?

TitleHypoxia-inducible factor-1: A molecular hint of physiological changes in the carotid body during long-term hypoxemia?
Authors
Issue Date2003
PublisherBentham Science Publishers Ltd.. The Journal's web site is located at http://www.bentham.org/cdtchd
Citation
Current Drug Targets - Cardiovascular And Haematological Disorders, 2003, v. 3 n. 3, p. 254-259 How to Cite?
AbstractThe aims of this review are to describe recent data focusing on the anatomical, functional and molecular changes of the carotid body during chronic hypoxemia, and to summarize current views in the literature relevant to the topic. The carotid body is the major peripheral sensor for detecting chemicals in the arterial blood. In acute hypoxia, carotid chemoreceptors transduce the signal to the brain for triggering reflexive responses of the cardiopulmonary system. The carotid body enlarges and changes its hypoxic sensitivity in humans and animals living at high altitude or subject to long-term hypoxemia associated with chronic cardiopulmonary diseases or hematological disorders. Recently, a surge of new evidence suggests that a heterodimeric transcriptional factor directly induced by severe tissue or cellular hypoxia, namely hypoxia-inducible factor-1 (HIF-1), is a key controller for the transcriptional regulation of the gene expression of a spectrum of proteins for the cellular response to hypoxia. These proteins, such as endothelin-1, type II nitric oxide synthase and vascular endothelial growth factor, play important physiological roles in the control of vascular tone and angiogenesis. In the carotid body, chronic hypoxemia induces remodeling of the vasculature, stimulates proliferation of the chemosensitive cells, and changes their excitability and sensitivity to chemical signals. In addition, HIF-1-targeted genes are expressed in the carotid body and the expression is modulated by chronic hypoxemia, suggesting an active role for HIF-1 in moderate levels of hypoxic stress.
Persistent Identifierhttp://hdl.handle.net/10722/81311
ISSN
References

 

DC FieldValueLanguage
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-09-06T08:16:13Z-
dc.date.available2010-09-06T08:16:13Z-
dc.date.issued2003en_HK
dc.identifier.citationCurrent Drug Targets - Cardiovascular And Haematological Disorders, 2003, v. 3 n. 3, p. 254-259en_HK
dc.identifier.issn1568-0061en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81311-
dc.description.abstractThe aims of this review are to describe recent data focusing on the anatomical, functional and molecular changes of the carotid body during chronic hypoxemia, and to summarize current views in the literature relevant to the topic. The carotid body is the major peripheral sensor for detecting chemicals in the arterial blood. In acute hypoxia, carotid chemoreceptors transduce the signal to the brain for triggering reflexive responses of the cardiopulmonary system. The carotid body enlarges and changes its hypoxic sensitivity in humans and animals living at high altitude or subject to long-term hypoxemia associated with chronic cardiopulmonary diseases or hematological disorders. Recently, a surge of new evidence suggests that a heterodimeric transcriptional factor directly induced by severe tissue or cellular hypoxia, namely hypoxia-inducible factor-1 (HIF-1), is a key controller for the transcriptional regulation of the gene expression of a spectrum of proteins for the cellular response to hypoxia. These proteins, such as endothelin-1, type II nitric oxide synthase and vascular endothelial growth factor, play important physiological roles in the control of vascular tone and angiogenesis. In the carotid body, chronic hypoxemia induces remodeling of the vasculature, stimulates proliferation of the chemosensitive cells, and changes their excitability and sensitivity to chemical signals. In addition, HIF-1-targeted genes are expressed in the carotid body and the expression is modulated by chronic hypoxemia, suggesting an active role for HIF-1 in moderate levels of hypoxic stress.en_HK
dc.languageengen_HK
dc.publisherBentham Science Publishers Ltd.. The Journal's web site is located at http://www.bentham.org/cdtchden_HK
dc.relation.ispartofCurrent Drug Targets - Cardiovascular and Haematological Disordersen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnoxia - metabolismen_HK
dc.subject.meshCarotid Body - metabolism - pathology - physiopathologyen_HK
dc.subject.meshChronic Diseaseen_HK
dc.subject.meshDNA-Binding Proteins - metabolismen_HK
dc.subject.meshEndothelin-1 - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHypoxia-Inducible Factor 1en_HK
dc.subject.meshHypoxia-Inducible Factor 1, alpha Subuniten_HK
dc.subject.meshNitric Oxide - biosynthesisen_HK
dc.subject.meshNitric Oxide Synthase - biosynthesisen_HK
dc.subject.meshNuclear Proteins - metabolismen_HK
dc.subject.meshReceptors, Endothelin - metabolismen_HK
dc.subject.meshReceptors, Vascular Endothelial Growth Factor - metabolismen_HK
dc.subject.meshTranscription Factorsen_HK
dc.subject.meshVascular Endothelial Growth Factor A - metabolismen_HK
dc.titleHypoxia-inducible factor-1: A molecular hint of physiological changes in the carotid body during long-term hypoxemia?en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1871-529X&volume=3&issue=3&spage=254&epage=259&date=2004&atitle=Hypoxia-inducible+factor-1:+a+molecular+hint+of+physiological+changes+in+the+carotid+body+during+long-term+hypoxemia?en_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2174/1568006033481447en_HK
dc.identifier.pmid12871043-
dc.identifier.scopuseid_2-s2.0-0041471553en_HK
dc.identifier.hkuros88100en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0041471553&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume3en_HK
dc.identifier.issue3en_HK
dc.identifier.spage254en_HK
dc.identifier.epage259en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK

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