Publication Name	World Journal of Diabetes
Manuscript ID	11481
Country	Japan

Received	2014-05-24 11:44
Peer-Review Started	2014-05-24 22:07
To Make the First Decision	2014-07-10 17:30
Return for Revision	2014-07-17 22:28
Revised	2014-07-24 11:42
Second Decision	2015-01-28 11:34
Accepted by Journal Editor-in-Chief	2015-01-29 10:41
Accepted by Company Editor-in-Chief	2015-02-09 09:48
Articles in Press	2015-02-09 09:48
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2015-04-13 14:02
Publish the Manuscript Online	2015-05-15 19:54

ISSN	1948-9358 (online)
Open Access	This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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Category	Medicine, Research & Experimental
Manuscript Type	Review
Article Title	How the kidney hyperfiltrates in diabetes: From molecules to hemodynamics
Manuscript Source	Invited Manuscript
All Author List	Tsuneo Takenaka, Tsutomu Inoue and Yusuke Watanabe
Funding Agency and Grant Number
Corresponding Author	Tsuneo Takenaka, MD, PhD, Professor, Department of Medicine, International University of Health and Welfare, Clinical Research Center, Sanno Hospital, 8-10-16 Akasaka Minato, Tokyo 107-0052, Japan. takenaka@iuhw.ac.jp
Key Words	Tubuloglomerular feedback; Salt paradox; Connexin; Glomerular hyperfiltration; Sodium-glucose co-transporter
Core Tip	A diminished tubuloglomerular feedback (TGF) in diabetes can explain both glomerular hyperfiltration and the activation of renin-angiotensin system. An enhanced absorption through sodium-glucose co-transporter in proximal tubule decreases the delivery to macula densa, reducing TGF signal generation in diabetes. Connexin phosphorylation and subsequent ubiquitination by oxidative stress in type 2 diabetes reduces its expression in juxtaglomerular apparatus, disabling TGF signal transduction. Clinical as well as experimental evidences support that this tubular hypothesis is working, and suggest that drugs targeting the above to normalize TGF, an intrinsic physiological system, would be effective to ameliorate diabetic nephropathy.
Publish Date	2015-05-15 19:54
Citation	Takenaka T, Inoue T, Watanabe Y. How the kidney hyperfiltrates in diabetes: From molecules to hemodynamics. World J Diabetes 2015; 6(4): 576-582
URL	http://www.wjgnet.com/1948-9358/full/v6/i4/576.htm
DOI	http://dx.doi.org/10.4239/wjd.v6.i4.576

Full Article (PDF)	WJD-6-576.pdf
Full Article (Word)	WJD-6-576.doc
Manuscript File	11481-Review.docx
Answering Reviewers	11481-Answering reviewers.pdf
Conflict-of-Interest Disclosure Form	11481-Conflict-of-interest statement.pdf
Copyright License Agreement	11481-Copyright assignment.pdf
Peer-review Report	11481-Peer-review(s) .pdf
Scientific Misconduct Check	11481-Scientific misconduct check.pdf
Scientific Editor Work List	11481-Scientific editor work list.pdf