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Article: The kallikrein-kinin system

TitleThe kallikrein-kinin system
Authors
Issue Date2011
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/CONEP
Citation
Contributions To Nephrology, 2011, v. 170, p. 145-155 How to Cite?
AbstractEmerging evidence suggests a role of the kallikrein-kinin system (KKS) in the pathogenesis of diabetic nephropathy (DN). Tissue kallikrein 1 is a member of the tissue kallikrein family that is mainly responsible for the generation of kinins, and bradykinin (BK) is the principal kinin responsible for the biologic actions of the KKS that acts through the ubiquitous BK 2receptor (B2R) and the inducible B1R. In the kidney, all KKS components are expressed. In particular, kallikrein 1 that is traditionally thought to be solely confined to the distal nephron has recently been identified in the proximal tubule of the human diabetic kidney. Current evidence suggests conflicting roles of the KKS in DN. For a renoprotective role of the KKS, BK reduces mesangial cell proliferation under the diabetic milieu; Akita B2R-/- or STZ-induced KLK-/- mice (T1DM) have more severe albuminuria and glomerulosclerosis, while antagonizing the B2R with icatibant attenuates the antiproteinuric effect of ramiprilin db/db mice (T2DM). For a detrimental role of the KKS, BK upregulates tubular cell IL-6, CCL-2, and TGF-β expression via ERK1/2 activation; the B2R- /- status protects against the development of DN lesions in STZ-injected mice, while blocking B2R with icatibant alleviates biochemical and histologic injuries in uninephrectomized db/db mice. These opposite findings may arise from multiple factors and call for further evaluation to clarify the role of the KKS in DN and diabetic tubulopathy. Copyright © 2011 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/137404
ISBN
ISSN
2015 Impact Factor: 2.438
2015 SCImago Journal Rankings: 0.494
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2011-08-26T14:24:27Z-
dc.date.available2011-08-26T14:24:27Z-
dc.date.issued2011en_HK
dc.identifier.citationContributions To Nephrology, 2011, v. 170, p. 145-155en_HK
dc.identifier.isbn978-3-8055-9742-5-
dc.identifier.issn0302-5144en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137404-
dc.description.abstractEmerging evidence suggests a role of the kallikrein-kinin system (KKS) in the pathogenesis of diabetic nephropathy (DN). Tissue kallikrein 1 is a member of the tissue kallikrein family that is mainly responsible for the generation of kinins, and bradykinin (BK) is the principal kinin responsible for the biologic actions of the KKS that acts through the ubiquitous BK 2receptor (B2R) and the inducible B1R. In the kidney, all KKS components are expressed. In particular, kallikrein 1 that is traditionally thought to be solely confined to the distal nephron has recently been identified in the proximal tubule of the human diabetic kidney. Current evidence suggests conflicting roles of the KKS in DN. For a renoprotective role of the KKS, BK reduces mesangial cell proliferation under the diabetic milieu; Akita B2R-/- or STZ-induced KLK-/- mice (T1DM) have more severe albuminuria and glomerulosclerosis, while antagonizing the B2R with icatibant attenuates the antiproteinuric effect of ramiprilin db/db mice (T2DM). For a detrimental role of the KKS, BK upregulates tubular cell IL-6, CCL-2, and TGF-β expression via ERK1/2 activation; the B2R- /- status protects against the development of DN lesions in STZ-injected mice, while blocking B2R with icatibant alleviates biochemical and histologic injuries in uninephrectomized db/db mice. These opposite findings may arise from multiple factors and call for further evaluation to clarify the role of the KKS in DN and diabetic tubulopathy. Copyright © 2011 S. Karger AG, Basel.en_HK
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/CONEPen_HK
dc.relation.ispartofContributions to Nephrologyen_HK
dc.rightsContributions to Nephrology. Copyright © S Karger AG.-
dc.subject.meshDiabetic Nephropathies - etiology-
dc.subject.meshExtracellular Signal-Regulated MAP Kinases - physiology-
dc.subject.meshKallikrein-Kinin System - physiology-
dc.subject.meshKidney Tubules, Proximal - metabolism-
dc.subject.meshReceptors, Bradykinin - physiology-
dc.titleThe kallikrein-kinin systemen_HK
dc.typeArticleen_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000325650en_HK
dc.identifier.pmid21659767-
dc.identifier.scopuseid_2-s2.0-79959204817en_HK
dc.identifier.hkuros190953en_US
dc.identifier.hkuros190728en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79959204817&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume170en_HK
dc.identifier.spage145en_HK
dc.identifier.epage155en_HK
dc.identifier.isiWOS:000292615800016-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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