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Article: Small lipid-binding proteins in regulating endothelial and vascular functions: Focusing on adipocyte fatty acid binding protein and lipocalin-2

TitleSmall lipid-binding proteins in regulating endothelial and vascular functions: Focusing on adipocyte fatty acid binding protein and lipocalin-2
Authors
Keywordsadipokine
atherosclerosis
drug discovery
endothelial cell
lipotoxicity
obesity
small lipid-binding protein
therapeutic targets
vascular inflammation
Issue Date2012
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2012, v. 165 n. 3, p. 603-621 How to Cite?
AbstractDysregulated production of adipokines from adipose tissue plays a critical role in the development of obesity-associated cardiovascular abnormalities. A group of adipokines, including adipocyte fatty acid binding protein (A-FABP) and lipocalin-2, possess specific lipid-binding activity and are up-regulated in obese human subjects and animal models. They act as lipid chaperones to promote lipotoxicity in endothelial cells and cause endothelial dysfunction under obese conditions. However, different small lipid-binding proteins modulate the development of vascular complications in distinctive manners, which are partly attributed to their specialized structural features and functionalities. By focusing on A-FABP and lipocalin-2, this review summarizes recent advances demonstrating the causative roles of these newly identified adipose tissue-derived lipid chaperones in obesity-related endothelial dysfunction and cardiovascular complications. The specific lipid-signalling mechanisms mediated by these two proteins are highlighted to support their specialized functions. In summary, A-FABP and lipocalin-2 represent potential therapeutic targets to design drugs for preventing vascular diseases associated with obesity. Linked Articles This article is part of a themed section on Fat and Vascular Responsiveness. To view the other articles in this section visit © 2011 The British Pharmacological Society.
Persistent Identifierhttp://hdl.handle.net/10722/139605
ISSN
2023 Impact Factor: 6.8
2023 SCImago Journal Rankings: 2.119
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council of Hong Kong777208 M
780410 M
HKU 2/07C
HKU4/CRF/10
Funding Information:

This work was supported by the General Research Fund (777208 M and 780410 M) and Collaborative Research Fund (HKU 2/07C and HKU4/CRF/10) from the Research Grant Council of Hong Kong.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.date.accessioned2011-09-23T05:52:28Z-
dc.date.available2011-09-23T05:52:28Z-
dc.date.issued2012en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2012, v. 165 n. 3, p. 603-621en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139605-
dc.description.abstractDysregulated production of adipokines from adipose tissue plays a critical role in the development of obesity-associated cardiovascular abnormalities. A group of adipokines, including adipocyte fatty acid binding protein (A-FABP) and lipocalin-2, possess specific lipid-binding activity and are up-regulated in obese human subjects and animal models. They act as lipid chaperones to promote lipotoxicity in endothelial cells and cause endothelial dysfunction under obese conditions. However, different small lipid-binding proteins modulate the development of vascular complications in distinctive manners, which are partly attributed to their specialized structural features and functionalities. By focusing on A-FABP and lipocalin-2, this review summarizes recent advances demonstrating the causative roles of these newly identified adipose tissue-derived lipid chaperones in obesity-related endothelial dysfunction and cardiovascular complications. The specific lipid-signalling mechanisms mediated by these two proteins are highlighted to support their specialized functions. In summary, A-FABP and lipocalin-2 represent potential therapeutic targets to design drugs for preventing vascular diseases associated with obesity. Linked Articles This article is part of a themed section on Fat and Vascular Responsiveness. To view the other articles in this section visit © 2011 The British Pharmacological Society.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_HK
dc.relation.ispartofBritish Journal of Pharmacologyen_HK
dc.rightsBritish Journal of Pharmacology. Copyright © John Wiley & Sons Ltd.-
dc.subjectadipokineen_HK
dc.subjectatherosclerosisen_HK
dc.subjectdrug discoveryen_HK
dc.subjectendothelial cellen_HK
dc.subjectlipotoxicityen_HK
dc.subjectobesityen_HK
dc.subjectsmall lipid-binding proteinen_HK
dc.subjecttherapeutic targetsen_HK
dc.subjectvascular inflammationen_HK
dc.titleSmall lipid-binding proteins in regulating endothelial and vascular functions: Focusing on adipocyte fatty acid binding protein and lipocalin-2en_HK
dc.typeArticleen_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1476-5381.2011.01528.xen_HK
dc.identifier.pmid21658023-
dc.identifier.pmcidPMC3315034-
dc.identifier.scopuseid_2-s2.0-84862907608en_HK
dc.identifier.hkuros195688en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84862907608&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume165en_HK
dc.identifier.issue3en_HK
dc.identifier.spage603en_HK
dc.identifier.epage621en_HK
dc.identifier.isiWOS:000298953100006-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.projectVascular dysfunction in obesity and diabetes: from risk prediction to therapeutic intervention-
dc.relation.projectA Multi-disciplinary Approach to Investigate Vascular Dysfunction in Obesity and Diabetes: From Molecular Mechanism to Therapeutic Intervention-
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.issnl0007-1188-

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