Journal of the American Society of Nephrology
2008 JASN IMPACT FACTOR 7.505 HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP 
    advanced
CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION


Published ahead of print on October 29, 2009
J Am Soc Nephrol 20: 2493-2502, 2009
© 2009 American Society of Nephrology
doi: 10.1681/ASN.2008111186

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
ASN.2008111186v1
ASN.2008111186v2
20/12/2493    most recent
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Google Scholar
Right arrow Articles by Lieberthal, W.
Right arrow Articles by Levine, J. S.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lieberthal, W.
Right arrow Articles by Levine, J. S.

Brief Reviews

The Role of the Mammalian Target Of Rapamycin (mTOR) in Renal Disease

Wilfred Lieberthal* and Jerrold S. Levine{dagger}

*Department of Medicine, Stony Brook University Medical Center, Stony Brook, and Department of Medicine, Northport Veterans Administration, Northport, New York; and
{dagger}Department of Medicine, University of Illinois at Chicago, and Department of Medicine, Jesse Brown Veterans Administration Hospital, Chicago, Illinois

Correspondence: Dr. Wilfred Lieberthal, Stony Brook Medical Center, Health Sciences Center, 16-081B, Nicholls Road, Stony Brook, NY 11794-8166; Phone: 631-444-1227; Fax: 631-444-6174; E-mail: wlieberthal{at}notes.cc.sunysb.edu

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that plays a pivotal role in mediating cell size and mass, proliferation, and survival. mTOR has also emerged as an important modulator of several forms of renal disease. mTOR is activated after acute kidney injury and contributes to renal regeneration and repair. Inhibition of mTOR with rapamycin delays recovery of renal function after acute kidney injury. Activation of mTOR within the kidney also occurs in animal models of diabetic nephropathy and other causes of progressive kidney disease. Rapamycin ameliorates several key mechanisms believed to mediate changes associated with the progressive loss of GFR in chronic kidney disease. These include glomerular hypertrophy, intrarenal inflammation, and interstitial fibrosis. mTOR also plays an important role in mediating cyst formation and enlargement in autosomal dominant polycystic kidney disease. Inhibition of mTOR by rapamycin or one of its analogues represents a potentially novel treatment for autosomal dominant polycystic kidney disease. Finally, inhibitors of mTOR improve survival in patients with metastatic renal cell carcinoma.







HOME CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION AUTHOR INFO
EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP