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- PMID: 22734110
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Article: The pathogenic role of the renal proximal tubular cell in diabetic nephropathy
Title | The pathogenic role of the renal proximal tubular cell in diabetic nephropathy |
---|---|
Authors | |
Keywords | db/db mice diabetic nephropathy fibrosis inflammation kallikrein-kinin system proximal tubular epithelial cell TLR4 KO mice toll-like receptor |
Issue Date | 2012 |
Publisher | Oxford 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? |
Abstract | A 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 Identifier | http://hdl.handle.net/10722/159646 |
ISSN | 2023 Impact Factor: 4.8 2023 SCImago Journal Rankings: 1.414 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Tang, SCW | en_HK |
dc.contributor.author | Lai, KN | en_HK |
dc.date.accessioned | 2012-08-16T05:53:42Z | - |
dc.date.available | 2012-08-16T05:53:42Z | - |
dc.date.issued | 2012 | en_HK |
dc.identifier.citation | Nephrology Dialysis Transplantation, 2012, v. 27 n. 8, p. 3049-3056 | en_HK |
dc.identifier.issn | 0931-0509 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/159646 | - |
dc.description.abstract | A 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.language | eng | en_US |
dc.publisher | Oxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/ | en_HK |
dc.relation.ispartof | Nephrology Dialysis Transplantation | en_HK |
dc.subject | db/db mice | en_HK |
dc.subject | diabetic nephropathy | en_HK |
dc.subject | fibrosis | en_HK |
dc.subject | inflammation | en_HK |
dc.subject | kallikrein-kinin system | en_HK |
dc.subject | proximal tubular epithelial cell | en_HK |
dc.subject | TLR4 KO mice | en_HK |
dc.subject | toll-like receptor | en_HK |
dc.title | The pathogenic role of the renal proximal tubular cell in diabetic nephropathy | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Tang, SCW: scwtang@hku.hk | en_HK |
dc.identifier.email | Lai, KN: knlai@hku.hk | en_HK |
dc.identifier.authority | Tang, SCW=rp00480 | en_HK |
dc.identifier.authority | Lai, KN=rp00324 | en_HK |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1093/ndt/gfs260 | en_HK |
dc.identifier.pmid | 22734110 | - |
dc.identifier.scopus | eid_2-s2.0-84864601012 | en_HK |
dc.identifier.hkuros | 203645 | en_US |
dc.identifier.hkuros | 22734110 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-84864601012&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 27 | en_HK |
dc.identifier.issue | 8 | en_HK |
dc.identifier.spage | 3049 | en_HK |
dc.identifier.epage | 3056 | en_HK |
dc.identifier.isi | WOS:000307173000012 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Tang, SCW=7403437082 | en_HK |
dc.identifier.scopusauthorid | Lai, KN=7402135706 | en_HK |
dc.identifier.citeulike | 10850747 | - |
dc.identifier.issnl | 0931-0509 | - |