AJP - Renal Information on EB 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Renal Physiol 294: F1265-F1272, 2008. First published February 20, 2008; doi:10.1152/ajprenal.00543.2007
0363-6127/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
294/6/F1265    most recent
00543.2007v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schmitt, R.
Right arrow Articles by Cantley, L. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schmitt, R.
Right arrow Articles by Cantley, L. G.

INVITED REVIEW

The impact of aging on kidney repair

Roland Schmitt1 and Lloyd G. Cantley2

2Section of Nephrology, Yale University School of Medicine, New Haven, Connecticut; and 1Department of Nephrology, Hannover Medical School, Hannover, Germany

Submitted 16 November 2007 ; accepted in final form 13 February 2008

The process of normal aging affects organ homeostasis as well as responses to acute and chronic injury. In view of the rapid growth in the elderly population, it is increasingly important for us to develop a mechanistic understanding of how these age-dependent changes can impact the susceptibility and response of the kidney to injurious stimuli. In this overview, we focus on the current understanding of those mechanisms by reviewing how cellular changes in the aging kidney might lead to a diminished proliferative reserve, an increased tendency for apoptosis, alterations in growth factor profiles, and changes in potential progenitor and immune cell functions. A better understanding of these processes may help us to define new targets for studying kidney repair and could ultimately lead to new therapeutic strategies that are specifically tailored for treatment of the elderly population.

growth factors; apoptosis; immune response



Address for reprint requests and other correspondence: L. G. Cantley, Yale Univ. School of Medicine, 333 Cedar Str. Box 208029, New Haven, CT 06520 (e-mail: lloyd.cantley{at}yale.edu)




This article has been cited by other articles:


Home page
J. Am. Soc. Nephrol.Home page
M. Naesens, E. Lerut, H. de Jonge, B. Van Damme, Y. Vanrenterghem, and D. R. J. Kuypers
Donor Age and Renal P-Glycoprotein Expression Associate with Chronic Histological Damage in Renal Allografts
J. Am. Soc. Nephrol., November 1, 2009; 20(11): 2468 - 2480.
[Abstract] [Full Text] [PDF]


Home page
CJASNHome page
M. Naesens, D. R. J. Kuypers, and M. Sarwal
Calcineurin Inhibitor Nephrotoxicity
Clin. J. Am. Soc. Nephrol., February 1, 2009; 4(2): 481 - 508.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
M. Wieser, G. Stadler, P. Jennings, B. Streubel, W. Pfaller, P. Ambros, C. Riedl, H. Katinger, J. Grillari, and R. Grillari-Voglauer
hTERT alone immortalizes epithelial cells of renal proximal tubules without changing their functional characteristics
Am J Physiol Renal Physiol, November 1, 2008; 295(5): F1365 - F1375.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.