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Article: Vascular effects of adiponectin: Molecular mechanisms and potential therapeutic intervention

TitleVascular effects of adiponectin: Molecular mechanisms and potential therapeutic intervention
Authors
KeywordsAdipokine
Adiponectin
Adiponectin receptor
Atherosclerosis
Cardiovascular disease
Diabetic complication
Endothelial dysfunction
Issue Date2008
PublisherPortland Press Ltd. The Journal's web site is located at http://www.clinsci.org/
Citation
Clinical Science, 2008, v. 114 n. 5-6, p. 361-374 How to Cite?
AbstractAdiponectin is a major adipocyte-secreted adipokine abundantly present in the circulation as three distinct oligomeric complexes. In addition to its role as an insulin sensitizer, mounting evidence suggests that adiponectin is an important player in maintaining vascular homoeostasis. Numerous epidemiological studies based on different ethnic groups have identified adiponectin deficiency (hypoadiponectinaemia) as an independent risk factor for endothelial dysfunction, hypertension, coronary heart disease, myocardial infarction and other cardiovascular complications. Conversely, elevation of circulating adiponectin concentrations by either genetic or pharmacological approaches can alleviate various vascular dysfunctions in animal models. Adiponectin exerts its vasculoprotective effects through its direct actions in the vascular system, such as increasing endothelial NO production, inhibiting endothelial cell activation and endothelium-leucocyte interaction, enhancing phagocytosis, and suppressing macrophage activation, macrophage-to-foam cell transformation and platelet aggregation. In addition, adiponectin reduces neointima formation through an oligomerization-dependent inhibition of smooth muscle proliferation. The present review highlights recent research advances in unveiling the molecular mechanisms that underpin the vascular actions of adiponectin and discusses the potential strategies of using adiponectin or its signalling pathways as therapeutic targets to combat obesity-related metabolic and vascular diseases. © The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/76757
ISSN
2015 Impact Factor: 4.996
2015 SCImago Journal Rankings: 2.427
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhu, Wen_HK
dc.contributor.authorCheng, KKYen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorXu, Aen_HK
dc.date.accessioned2010-09-06T07:24:36Z-
dc.date.available2010-09-06T07:24:36Z-
dc.date.issued2008en_HK
dc.identifier.citationClinical Science, 2008, v. 114 n. 5-6, p. 361-374en_HK
dc.identifier.issn0143-5221en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76757-
dc.description.abstractAdiponectin is a major adipocyte-secreted adipokine abundantly present in the circulation as three distinct oligomeric complexes. In addition to its role as an insulin sensitizer, mounting evidence suggests that adiponectin is an important player in maintaining vascular homoeostasis. Numerous epidemiological studies based on different ethnic groups have identified adiponectin deficiency (hypoadiponectinaemia) as an independent risk factor for endothelial dysfunction, hypertension, coronary heart disease, myocardial infarction and other cardiovascular complications. Conversely, elevation of circulating adiponectin concentrations by either genetic or pharmacological approaches can alleviate various vascular dysfunctions in animal models. Adiponectin exerts its vasculoprotective effects through its direct actions in the vascular system, such as increasing endothelial NO production, inhibiting endothelial cell activation and endothelium-leucocyte interaction, enhancing phagocytosis, and suppressing macrophage activation, macrophage-to-foam cell transformation and platelet aggregation. In addition, adiponectin reduces neointima formation through an oligomerization-dependent inhibition of smooth muscle proliferation. The present review highlights recent research advances in unveiling the molecular mechanisms that underpin the vascular actions of adiponectin and discusses the potential strategies of using adiponectin or its signalling pathways as therapeutic targets to combat obesity-related metabolic and vascular diseases. © The Authors.en_HK
dc.languageengen_HK
dc.publisherPortland Press Ltd. The Journal's web site is located at http://www.clinsci.org/en_HK
dc.relation.ispartofClinical Scienceen_HK
dc.subjectAdipokineen_HK
dc.subjectAdiponectinen_HK
dc.subjectAdiponectin receptoren_HK
dc.subjectAtherosclerosisen_HK
dc.subjectCardiovascular diseaseen_HK
dc.subjectDiabetic complicationen_HK
dc.subjectEndothelial dysfunctionen_HK
dc.subject.meshAdiponectin - deficiency - hysiology - therapeutic use-
dc.subject.meshVascular Diseases - physiopathology - prevention & control-
dc.subject.meshAnimals-
dc.subject.meshAntioxidants - therapeutic use-
dc.subject.meshEndothelium, Vascular - metabolism-
dc.titleVascular effects of adiponectin: Molecular mechanisms and potential therapeutic interventionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-5221&volume=114&spage=361&epage=374&date=2008&atitle=Vascular+effects+of+adiponectin:+molecular+mechanisms+and+potential+therapeutic+interventionen_HK
dc.identifier.emailCheng, KKY: dorncky@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.authorityCheng, KKY=rp01672en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1042/CS20070347en_HK
dc.identifier.pmid18230060-
dc.identifier.scopuseid_2-s2.0-39549094717en_HK
dc.identifier.hkuros157714en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-39549094717&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume114en_HK
dc.identifier.issue5-6en_HK
dc.identifier.spage361en_HK
dc.identifier.epage374en_HK
dc.identifier.isiWOS:000253849000002-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridZhu, W=7404232544en_HK
dc.identifier.scopusauthoridCheng, KKY=7402997599en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK

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