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Article: The renin-angiotensin system

TitleThe renin-angiotensin 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. 135-144 How to Cite?
AbstractDiabetic nephropathy (DN) is a leading cause of end-stage renal disease in developed countries where type 2 diabetes mellitus has reached epidemic proportions. Although the exact pathogenesis of DN is not fully understood and is likely diverse in nature, there are convincing data that the renin-angiotensin system (RAS) is a major mediator of renal injury. Angiotensin II (Ang II), traditionally playing a central role as a mediator of glomerular hemodynamic adaptation and injury, is now recognized to exert proinflammatory action leading to upregulation of chemokines, adhesion molecules, and other fibrogenic growth factors that culminate in a decline of renal function. Hyperglycemia and mechanical stress deriving from glomerular hypertension are the key factors underlying pathogenesis of DN. The common signaling pathways stimulated by high glucose and mechanical insult may act synergistically, thereby accelerating the cell damage. Podocytes are subjected not only to the load of filtered glucose but also to diverse mechanical forces. Both high glucose and mechanical stress may impair the protein systems anchoring the podocyte foot processes in the glomerular basement membrane, therefore blunting resistance of these cells to mechanical forces in addition to the inflammatory insults. Loss of the podocytes is irreversible due to their inability to proliferate and to replenish damaged cells. Podocytes are injured early in the course of DN, which, most likely, underlies further glomerular and renal damage in diabetes. Under normal physiological conditions, podocytes play a specific role in the maintenance of intraglomerular RAS balance with enzymatic activities that predominantly lead to ANG1-7 and ANG1-9 formation, as well as Ang II degradation. ANG1-7 counteracts the proinflammatory actions of Ang II. These enzymatic activities are altered in a nonphysiological environment such as hyperglycemia that mimics diabetic kidney disease. An understanding of the local intraglomerular RAS will provide a novel approach for early stages of DN. Copyright © 2011 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/137406
ISSN
2015 Impact Factor: 2.438
2015 SCImago Journal Rankings: 0.494
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorTang, SCWen_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. 135-144en_HK
dc.identifier.issn0302-5144en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137406-
dc.description.abstractDiabetic nephropathy (DN) is a leading cause of end-stage renal disease in developed countries where type 2 diabetes mellitus has reached epidemic proportions. Although the exact pathogenesis of DN is not fully understood and is likely diverse in nature, there are convincing data that the renin-angiotensin system (RAS) is a major mediator of renal injury. Angiotensin II (Ang II), traditionally playing a central role as a mediator of glomerular hemodynamic adaptation and injury, is now recognized to exert proinflammatory action leading to upregulation of chemokines, adhesion molecules, and other fibrogenic growth factors that culminate in a decline of renal function. Hyperglycemia and mechanical stress deriving from glomerular hypertension are the key factors underlying pathogenesis of DN. The common signaling pathways stimulated by high glucose and mechanical insult may act synergistically, thereby accelerating the cell damage. Podocytes are subjected not only to the load of filtered glucose but also to diverse mechanical forces. Both high glucose and mechanical stress may impair the protein systems anchoring the podocyte foot processes in the glomerular basement membrane, therefore blunting resistance of these cells to mechanical forces in addition to the inflammatory insults. Loss of the podocytes is irreversible due to their inability to proliferate and to replenish damaged cells. Podocytes are injured early in the course of DN, which, most likely, underlies further glomerular and renal damage in diabetes. Under normal physiological conditions, podocytes play a specific role in the maintenance of intraglomerular RAS balance with enzymatic activities that predominantly lead to ANG1-7 and ANG1-9 formation, as well as Ang II degradation. ANG1-7 counteracts the proinflammatory actions of Ang II. These enzymatic activities are altered in a nonphysiological environment such as hyperglycemia that mimics diabetic kidney disease. An understanding of the local intraglomerular RAS will provide a novel approach for early stages of DN. 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 - physiopathology-
dc.subject.meshPodocytes - metabolism-
dc.subject.meshPolymorphism, Genetic-
dc.subject.meshReceptor, Angiotensin, Type 2 - physiology-
dc.subject.meshRenin-Angiotensin System - genetics - physiology-
dc.titleThe renin-angiotensin systemen_HK
dc.typeArticleen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000325649en_HK
dc.identifier.pmid21659766-
dc.identifier.scopuseid_2-s2.0-79959219641en_HK
dc.identifier.hkuros190799en_US
dc.identifier.hkuros196741en_US
dc.identifier.hkuros190948en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79959219641&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume170en_HK
dc.identifier.spage135en_HK
dc.identifier.epage144en_HK
dc.identifier.isiWOS:000292615800015-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK

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