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Article: Molecular basis of IgA nephropathy

TitleMolecular basis of IgA nephropathy
Authors
KeywordsAngiotensin II receptors
Electrostatic charge
Growth factors
IgA
IgA nephropathy
Mesangial inflammation
Renin-angiotensin system
Tubulointerstitial injury
Issue Date2005
PublisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cmm/index.htm
Citation
Current Molecular Medicine, 2005, v. 5 n. 5, p. 475-487 How to Cite?
AbstractIgA nephropathy (IgAN) is the most common glomerulonephritis worldwide and remains an important cause of end-stage renal failure. However, the basic molecular mechanism(s) underlying abnormal IgA synthesis, selective mesangial deposition with ensuing mesangial cell proliferation and extracellular matrix expansion remains poorly understood. Notably, the severity of tubulointerstitial lesions better predicts the renal progression than the degree of glomerular lesions. The task of elucidating the molecular basis of IgAN is made especially challenging by the fact that both environmental and genetic components likely contribute to the development and progression of IgAN. This review will summarize the earlier works on the structure of the IgA molecule, mechanisms of mesangial IgA deposition and pathophysiologic effects of IgA on mesangial cells following mesangial deposition. Recently, a series of important advances in the area of communication between the glomerular mesangium and renal tubular cells have emerged. These novel findings regarding the molecular pathogenesis of IgAN will be helpful in designing future directions for therapy. © 2005 Bentham Science Publishers Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/77942
ISSN
2015 Impact Factor: 2.912
2015 SCImago Journal Rankings: 1.574
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, ASHen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:37:26Z-
dc.date.available2010-09-06T07:37:26Z-
dc.date.issued2005en_HK
dc.identifier.citationCurrent Molecular Medicine, 2005, v. 5 n. 5, p. 475-487en_HK
dc.identifier.issn1566-5240en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77942-
dc.description.abstractIgA nephropathy (IgAN) is the most common glomerulonephritis worldwide and remains an important cause of end-stage renal failure. However, the basic molecular mechanism(s) underlying abnormal IgA synthesis, selective mesangial deposition with ensuing mesangial cell proliferation and extracellular matrix expansion remains poorly understood. Notably, the severity of tubulointerstitial lesions better predicts the renal progression than the degree of glomerular lesions. The task of elucidating the molecular basis of IgAN is made especially challenging by the fact that both environmental and genetic components likely contribute to the development and progression of IgAN. This review will summarize the earlier works on the structure of the IgA molecule, mechanisms of mesangial IgA deposition and pathophysiologic effects of IgA on mesangial cells following mesangial deposition. Recently, a series of important advances in the area of communication between the glomerular mesangium and renal tubular cells have emerged. These novel findings regarding the molecular pathogenesis of IgAN will be helpful in designing future directions for therapy. © 2005 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/cmm/index.htmen_HK
dc.relation.ispartofCurrent Molecular Medicineen_HK
dc.subjectAngiotensin II receptorsen_HK
dc.subjectElectrostatic chargeen_HK
dc.subjectGrowth factorsen_HK
dc.subjectIgAen_HK
dc.subjectIgA nephropathyen_HK
dc.subjectMesangial inflammationen_HK
dc.subjectRenin-angiotensin systemen_HK
dc.subjectTubulointerstitial injuryen_HK
dc.titleMolecular basis of IgA nephropathyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1566-5240&volume=5&issue=5&spage=475&epage=487&date=2005&atitle=Molecular+basis+of+IgA+nephropathyen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2174/1566524054553450en_HK
dc.identifier.pmid16101476-
dc.identifier.scopuseid_2-s2.0-23144444250en_HK
dc.identifier.hkuros121459en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23144444250&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume5en_HK
dc.identifier.issue5en_HK
dc.identifier.spage475en_HK
dc.identifier.epage487en_HK
dc.identifier.isiWOS:000230747200004-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridLai, ASH=8711668800en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.citeulike267100-

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