Literature DB >> 17554351

Diabetic nephropathy and proximal tubule ROS: challenging our glomerulocentricity.

S P Bagby1.   

Abstract

Diabetic nephropathy is currently viewed as a predominantly glomerular process with glomerular injury driving secondary tubular loss. Brezniceanu and colleagues apply transgenic methods to support a prominent role for reactive oxygen species as mediators and for the proximal tubule as a major site of early disease activity in diabetes. Results support evidence for early tubular apoptosis and atrophy in human diabetic nephropathy.

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Year:  2007        PMID： 17554351     DOI： 10.1038/sj.ki.5002286

Source DB:  PubMed          Journal:  Kidney Int        ISSN： 0085-2538            Impact factor:   10.612


  19 in total

1.  Renal tubular ACE-mediated tubular injury is the major contributor to microalbuminuria in early diabetic nephropathy.

Authors:  Masahiro Eriguchi; Mercury Lin; Michifumi Yamashita; Tuantuan V Zhao; Zakir Khan; Ellen A Bernstein; Susan B Gurley; Romer A Gonzalez-Villalobos; Kenneth E Bernstein; Jorge F Giani
Journal:  Am J Physiol Renal Physiol       Date:  2017-11-29

2.  Reactive oxygen species promote caspase-12 expression and tubular apoptosis in diabetic nephropathy.

Authors:  Marie-Luise Brezniceanu; Cara J Lau; Nicolas Godin; Isabelle Chénier; Alain Duclos; Jean Ethier; Janos G Filep; Julie R Ingelfinger; Shao-Ling Zhang; John S D Chan
Journal:  J Am Soc Nephrol       Date:  2010-03-18       Impact factor: 10.121

Review 3.  Oxidative stress in early diabetic nephropathy: fueling the fire.

Authors:  Dhruv K Singh; Peter Winocour; Ken Farrington
Journal:  Nat Rev Endocrinol       Date:  2010-12-14       Impact factor: 43.330

4.  Radix Astragali lowers kidney oxidative stress in diabetic rats treated with insulin.

Authors:  Y Gao; R R Zhang; J H Li; M Ren; Z X Ren; J H Shi; Q Z Pan; S P Ren
Journal:  Endocrine       Date:  2012-04-20       Impact factor: 3.633

Review 5.  The proximal tubule is the primary target of injury and progression of kidney disease: role of the glomerulotubular junction.

Authors:  Robert L Chevalier
Journal:  Am J Physiol Renal Physiol       Date:  2016-05-18

6.  Aquaporin 11 insufficiency modulates kidney susceptibility to oxidative stress.

Authors:  Elena N Atochina-Vasserman; Asel Biktasova; Elena Abramova; Dong-Sheng Cheng; Vasiliy V Polosukhin; Harikrishna Tanjore; Saki Takahashi; Hiroko Sonoda; Liberty Foye; Christo Venkov; Sergey V Ryzhov; Sergey Novitskiy; Natalia Shlonimskaya; Masahiro Ikeda; Timothy S Blackwell; William E Lawson; Andrew J Gow; Raymond C Harris; Mikhail M Dikov; Elena E Tchekneva
Journal:  Am J Physiol Renal Physiol       Date:  2013-03-13

7.  Enhanced expressions of sodium-glucose cotransporters in the kidneys of diabetic Zucker rats.

Authors:  Niloofar M Tabatabai; Mukut Sharma; Samuel S Blumenthal; David H Petering
Journal:  Diabetes Res Clin Pract       Date:  2008-12-17       Impact factor: 5.602

8.  Early-outgrowth bone marrow cells attenuate renal injury and dysfunction via an antioxidant effect in a mouse model of type 2 diabetes.

Authors:  Yanling Zhang; Darren A Yuen; Andrew Advani; Kerri Thai; Suzanne L Advani; David Kepecs; M Golam Kabir; Kim A Connelly; Richard E Gilbert
Journal:  Diabetes       Date:  2012-05-17       Impact factor: 9.461

9.  CYP24A1 exacerbated activity during diabetes contributes to kidney tubular apoptosis via caspase-3 increased expression and activation.

Authors:  Alexandre Tourigny; Frédrick Charbonneau; Paul Xing; Rania Boukrab; Guy Rousseau; René St-Arnaud; Marie-Luise Brezniceanu
Journal:  PLoS One       Date:  2012-10-31       Impact factor: 3.240

10.  Sodium-glucose cotransporter inhibition prevents oxidative stress in the kidney of diabetic rats.

Authors:  Horacio Osorio; Israel Coronel; Abraham Arellano; Ursino Pacheco; Rocío Bautista; Martha Franco; Bruno Escalante
Journal:  Oxid Med Cell Longev       Date:  2012-11-20       Impact factor: 6.543
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