Nuclear receptors in renal disease.
Authors Levi M
Submitted By Moshe Levi on 2/22/2012
Status Published
Journal Biochimica et biophysica acta
Year 2011
Date Published 8/1/2011
Volume : Pages 1812 : 1061 - 1067
PubMed Reference 21511032
Abstract Diabetes is the leading cause of end-stage renal disease in developed countries.
In spite of excellent glucose and blood pressure control, including
administration of angiotensin converting enzyme inhibitors and/or angiotensin II
receptor blockers, diabetic nephropathy still develops and progresses. The
development of additional protective therapeutic interventions is, therefore, a
major priority. Nuclear hormone receptors regulate carbohydrate metabolism,
lipid metabolism, the immune response, and inflammation. These receptors also
modulate the development of fibrosis. As a result of their diverse biological
effects, nuclear hormone receptors have become major pharmaceutical targets for
the treatment of metabolic diseases. The increasing prevalence of diabetic
nephropathy has led intense investigation into the role that nuclear hormone
receptors may have in slowing or preventing the progression of renal disease.
This role of nuclear hormone receptors would be associated with improvements in
metabolism, the immune response, and inflammation. Several nuclear receptor
activating ligands (agonists) have been shown to have a renal protective effect
in the context of diabetic nephropathy. This review will discuss the evidence
regarding the beneficial effects of the activation of several nuclear,
especially the vitamin D receptor (VDR), farnesoid X receptor (FXR), and
peroxisome-proliferator-associated receptors (PPARs) in preventing the
progression of diabetic nephropathy and describe how the discovery and
development of compounds that modulate the activity of nuclear hormone receptors
may provide potential additional therapeutic approaches in the management of
diabetic nephropathy. This article is part of a Special Issue entitled:
Translating nuclear receptors from health to disease.

Investigators with authorship
Moshe LeviGeorgetown University