Skip Navigation


NDT Advance Access originally published online on February 11, 2009
Nephrology Dialysis Transplantation 2009 24(5):1373-1377; doi:10.1093/ndt/gfp028
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
24/5/1373    most recent
gfp028v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Miyata, T.
Right arrow Articles by van Ypersele de Strihou, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Miyata, T.
Right arrow Articles by van Ypersele de Strihou, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Translation of basic science into clinical medicine: novel targets for diabetic nephropathy

Toshio Miyata and Charles van Ypersele de Strihou

Center for Translational and Advanced Research, Tohoku University Graduate School of Medicine, Sendai, Japan Service de Nephrologie, Universite Catholique de Louvain, Brussels, Belgium

Correspondence and offprint requests to: Toshio Miyata, Center for Translational and Advanced Research, Tohoku University Graduate School of Medicine, 2-1 Seiryo-Machi, Aoba-ku, Sendai, Miyagi 980-8575, Japan. Tel: +81-22-717-8157; E-mail: t-miyata@mail.tains.tohoku.ac.jp

Keywords: hypertension; hypoxia; metabolic syndrome; oxidative stress; PAI-1

The first 150 words of the full text of this article appear below.

Despite major therapeutic advances, the incidence of diabetic nephropathy remains worrisome. Classical factors contributing to its pathology (e.g. hypertension, hyperglycaemia, hyperinsulinaemia, and hyperlipidaemia) are now amenable to treatment, but current therapies do not fully prevent renal complications. The experimental study of animals has recently incriminated newer culprits, such as hypoxia, oxidative stress, advanced glycation, etc. and identified several target molecules. These progresses remain to be translated into clinical medicine.



   Lessons of animal experiments for current therapies in humans
 
SHR/NDmcr-cp is a hypertensive rat strain derived from the spontaneously hypertensive rat (SHR). As a result of an additional mutation of the leptin receptor, it develops obesity, hyperglycaemia, hyperinsulinaemia and hyperlipidaemia, all of which characterize human type 2 diabetes mellitus [1,2]. As anticipated, significant renal damage ensues. We utilized this model to evaluate several current therapeutic approaches.

Dietary correction of obesity
Restriction of the caloric intake of SHR/NDmcr-cp by 30% for 20 weeks corrected both obesity and hyperlipidaemia but failed to change blood . . . [Full Text of this Article]

Normalization of blood pressure
Control of hyperglycaemia/hyperinsulinaemia


   Novel therapeutic targets
 
Hypoxia correction
Inhibition of advanced glycation
Plasminogen activator inhibitor (PAI)-1


   Conclusion
 

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
A. Nishiyama, T. Matsusaka, and T. Miyata
Angiotensin II type 1A receptor deficiency and longevity
Nephrol. Dial. Transplant., November 1, 2009; 24(11): 3280 - 3281.
[Full Text] [PDF]