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PPAR Research
Volume 2008, Article ID 183108, 9 pages
Review Article

PPAR in Kidney Physiology and Pathophysiology

1Department of Biochemistry and Molecular Biology, Medical and Health Science Center, University of Debrecen, Nagyerdei krt. 98, 4012 Debrecen, Hungary
2Research Group of Apoptosis and Genomics, Hungarian Academy of Sciences, Nagyerdei krt. 98, 4012 Debrecen, Hungary

Received 29 August 2008; Accepted 17 December 2008

Academic Editor: Xiong Ruan

Copyright © 2008 Éva Kiss-Tóth and Tamás Rőszer. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Involvement of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR ) in kidney physiology has been explored recently. Synthetic PPAR ligands can ameliorate the diabetic kidney disease through different mechanisms, involving inhibition of mesangial cell growth, reduction of mesangial matrix, and cytokine production of glomerular cells as well as promoting endothelial cell survival within the kidney glomeruli. Activation of PPAR has additional profibrotic consequences, which can contribute to wound healing in diabetic glomerulonephritis. Beside many beneficial effects, PPAR activation, however, can lead to severe water retention, a common side effect of thiazolidinedione therapy. This unwanted effect is due to the activation of PPAR in the mesonephric distal collecting system, where PPAR positively regulates sodium and water resorbtion leading to the expansion of interstitial fluid volume. Recent studies indicate that PPAR is also involved in the normal kidney development, renal lipid metabolism, and activation of the renin-angiotensin system. In this paper, we give a synopsis of the current knowledge on PPAR functions in kidney phyisology and pathophysiology.