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Article: The pathogenic role of the renal proximal tubular cell in diabetic nephropathy

TitleThe pathogenic role of the renal proximal tubular cell in diabetic nephropathy
Authors
Keywordsdb/db mice
diabetic nephropathy
fibrosis
inflammation
kallikrein-kinin system
proximal tubular epithelial cell
TLR4 KO mice
toll-like receptor
Issue Date2012
PublisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/
Citation
Nephrology Dialysis Transplantation, 2012, v. 27 n. 8, p. 3049-3056 How to Cite?
AbstractA growing body of evidence indicates that the renal proximal tubular epithelial cell (PTEC) plays an important role in the pathogenesis of diabetic nephropathy (DN). Microalbuminuria that intensifies over time to overt proteinuria, a hallmark of DN, is already known to activate the PTEC to induce tubulointerstitial inflammation. In addition to proteins, a number of diabetic substrates including high glucose per se, advanced glycation end-products and their carbonyl intermediates, angiotensin II, and ultrafiltered growth factors activate a number of signaling pathways including nuclear factor kappa B, protein kinase C, extracellular signal-regulated kinase 1/2, p38, signal transducer and activator of transcription-1 and the generation of reactive oxygen species, to culminate in tubular cell hypertrophy and the accumulation in the interstitium of a repertoire of chemokines, cytokines, growth factors and adhesion molecules capable of orchestrating further inflammation and fibrosis. More recently, the kallikrein-kinin system (KKS) and toll-like receptors (TLRs) in PTECs have been implicated in this process. While in vitro data suggest that the KKS contributes to the progression of DN, there are conflicting in vivo results on its precise role, which may in part be strain-dependent. On the other hand, there are both in vitro and in vivo data to suggest a role for both TLR2 and TLR4 in DN. In this review, we offer a critical appraisal of the events linking the participation of the PTEC to the pathogenesis of DN, which we believe may be collectively termed diabetic tubulopathy. © The Author 2012. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/159646
ISSN
2015 Impact Factor: 4.085
2015 SCImago Journal Rankings: 1.780
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2012-08-16T05:53:42Z-
dc.date.available2012-08-16T05:53:42Z-
dc.date.issued2012en_HK
dc.identifier.citationNephrology Dialysis Transplantation, 2012, v. 27 n. 8, p. 3049-3056en_HK
dc.identifier.issn0931-0509en_HK
dc.identifier.urihttp://hdl.handle.net/10722/159646-
dc.description.abstractA growing body of evidence indicates that the renal proximal tubular epithelial cell (PTEC) plays an important role in the pathogenesis of diabetic nephropathy (DN). Microalbuminuria that intensifies over time to overt proteinuria, a hallmark of DN, is already known to activate the PTEC to induce tubulointerstitial inflammation. In addition to proteins, a number of diabetic substrates including high glucose per se, advanced glycation end-products and their carbonyl intermediates, angiotensin II, and ultrafiltered growth factors activate a number of signaling pathways including nuclear factor kappa B, protein kinase C, extracellular signal-regulated kinase 1/2, p38, signal transducer and activator of transcription-1 and the generation of reactive oxygen species, to culminate in tubular cell hypertrophy and the accumulation in the interstitium of a repertoire of chemokines, cytokines, growth factors and adhesion molecules capable of orchestrating further inflammation and fibrosis. More recently, the kallikrein-kinin system (KKS) and toll-like receptors (TLRs) in PTECs have been implicated in this process. While in vitro data suggest that the KKS contributes to the progression of DN, there are conflicting in vivo results on its precise role, which may in part be strain-dependent. On the other hand, there are both in vitro and in vivo data to suggest a role for both TLR2 and TLR4 in DN. In this review, we offer a critical appraisal of the events linking the participation of the PTEC to the pathogenesis of DN, which we believe may be collectively termed diabetic tubulopathy. © The Author 2012. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.en_HK
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/en_HK
dc.relation.ispartofNephrology Dialysis Transplantationen_HK
dc.subjectdb/db miceen_HK
dc.subjectdiabetic nephropathyen_HK
dc.subjectfibrosisen_HK
dc.subjectinflammationen_HK
dc.subjectkallikrein-kinin systemen_HK
dc.subjectproximal tubular epithelial cellen_HK
dc.subjectTLR4 KO miceen_HK
dc.subjecttoll-like receptoren_HK
dc.titleThe pathogenic role of the renal proximal tubular cell in diabetic nephropathyen_HK
dc.typeArticleen_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/ndt/gfs260en_HK
dc.identifier.pmid22734110-
dc.identifier.scopuseid_2-s2.0-84864601012en_HK
dc.identifier.hkuros203645en_US
dc.identifier.hkuros22734110-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84864601012&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume27en_HK
dc.identifier.issue8en_HK
dc.identifier.spage3049en_HK
dc.identifier.epage3056en_HK
dc.identifier.isiWOS:000307173000012-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.citeulike10850747-

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