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Article: Expression and functions of vasoactive substances regulated by hypoxia-inducible factor-1 in chronic hypoxemia

TitleExpression and functions of vasoactive substances regulated by hypoxia-inducible factor-1 in chronic hypoxemia
Authors
KeywordsChronic hypoxia
Endothelin
HIF
Nitric oxide
VEGF
Issue Date2006
PublisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cmccha/
Citation
Cardiovascular And Hematological Agents In Medicinal Chemistry, 2006, v. 4 n. 3, p. 199-218 How to Cite?
AbstractThe aims of the present review are to summarize and to discuss the role of hypoxia-inducible factor-1 (HIF-1) and the expression and functions of vasoactive substances in chronic hypoxemia with specific focus in the liver and the carotid body. Vascular remodelling and vasoactive substances play important functional roles in the adaptive response to chronic hypoxemia for the maintenance of oxygen homeostasis in all systems in man. HIF-1 regulates the gene expression of vasoactive substances such as vascular endothelial growth factor (VEGF), endothelin-1 (ET-1) and enzymes for producing nitric oxide (NO). Recent studies have shown the effect of chronic hypoxia on the expression of HIF-1α and HIF-1-target genes in multiple organ systems including the liver and the carotid body. Results are consistent with increases in the hematocrit levels, pulmonary arterial pressure and right heart mass developed during chronic hypoxia. In addition, the carotid body is also hyperplastic and increases in organ mass with increased levels of HIF-1α and the vasoactive substances. These molecules increase the mitotic activity and modulate the excitability of the chemoreceptor. Intriguingly, the liver morphology, serum alanine aminotransferase and 8-isoprostane levels are within normal range in chronic hypoxia, suggesting the absence of significant oxidative stress. Yet, the HIF-1α is upregulated and the mRNA and protein levels of VEGF, ET-1, inducible and constitutive NO synthases are elevated in the liver during chronic hypoxia. In conclusion, the adaptive response to long-term hypoxemia involves compensatory mechanisms mediated by expressing significant levels of HIF-1α and vasoactive substances regulated by HIF-1. © 2006 Bentham Science Publishers Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/67931
ISSN
2015 SCImago Journal Rankings: 0.486
References

 

DC FieldValueLanguage
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorLau, TYHen_HK
dc.contributor.authorNanji, AAen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-09-06T05:59:34Z-
dc.date.available2010-09-06T05:59:34Z-
dc.date.issued2006en_HK
dc.identifier.citationCardiovascular And Hematological Agents In Medicinal Chemistry, 2006, v. 4 n. 3, p. 199-218en_HK
dc.identifier.issn1871-5257en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67931-
dc.description.abstractThe aims of the present review are to summarize and to discuss the role of hypoxia-inducible factor-1 (HIF-1) and the expression and functions of vasoactive substances in chronic hypoxemia with specific focus in the liver and the carotid body. Vascular remodelling and vasoactive substances play important functional roles in the adaptive response to chronic hypoxemia for the maintenance of oxygen homeostasis in all systems in man. HIF-1 regulates the gene expression of vasoactive substances such as vascular endothelial growth factor (VEGF), endothelin-1 (ET-1) and enzymes for producing nitric oxide (NO). Recent studies have shown the effect of chronic hypoxia on the expression of HIF-1α and HIF-1-target genes in multiple organ systems including the liver and the carotid body. Results are consistent with increases in the hematocrit levels, pulmonary arterial pressure and right heart mass developed during chronic hypoxia. In addition, the carotid body is also hyperplastic and increases in organ mass with increased levels of HIF-1α and the vasoactive substances. These molecules increase the mitotic activity and modulate the excitability of the chemoreceptor. Intriguingly, the liver morphology, serum alanine aminotransferase and 8-isoprostane levels are within normal range in chronic hypoxia, suggesting the absence of significant oxidative stress. Yet, the HIF-1α is upregulated and the mRNA and protein levels of VEGF, ET-1, inducible and constitutive NO synthases are elevated in the liver during chronic hypoxia. In conclusion, the adaptive response to long-term hypoxemia involves compensatory mechanisms mediated by expressing significant levels of HIF-1α and vasoactive substances regulated by HIF-1. © 2006 Bentham Science Publishers Ltd.en_HK
dc.languageengen_HK
dc.publisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cmccha/en_HK
dc.relation.ispartofCardiovascular and Hematological Agents in Medicinal Chemistryen_HK
dc.subjectChronic hypoxiaen_HK
dc.subjectEndothelinen_HK
dc.subjectHIFen_HK
dc.subjectNitric oxideen_HK
dc.subjectVEGFen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnoxia - genetics - physiopathologyen_HK
dc.subject.meshCarotid Arteries - metabolismen_HK
dc.subject.meshChronic Diseaseen_HK
dc.subject.meshEndothelin-1 - metabolism - physiologyen_HK
dc.subject.meshErythropoietin - metabolism - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHypoxia-Inducible Factor 1 - genetics - physiologyen_HK
dc.subject.meshLiver - physiopathologyen_HK
dc.subject.meshNitric Oxide - metabolism - physiologyen_HK
dc.subject.meshOxygen - metabolismen_HK
dc.subject.meshTranscription Factors - metabolism - physiologyen_HK
dc.subject.meshVascular Endothelial Growth Factor A - metabolism - physiologyen_HK
dc.titleExpression and functions of vasoactive substances regulated by hypoxia-inducible factor-1 in chronic hypoxemiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1871-5257&volume=4&spage=199&epage=218&date=2006&atitle=Expression+and+functions+of+vasoactive+substances+regulated+by+hypoxia-inducible+factor-1+in+chronic+hypoxemiaen_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2174/187152506777698290en_HK
dc.identifier.pmid16842206-
dc.identifier.scopuseid_2-s2.0-33745967486en_HK
dc.identifier.hkuros116641en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745967486&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue3en_HK
dc.identifier.spage199en_HK
dc.identifier.epage218en_HK
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridLau, TYH=26323763000en_HK
dc.identifier.scopusauthoridNanji, AA=35885060300en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK

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