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Publication
Nuclear hormone receptors in diabetic nephropathy.
Authors
Wang XX, Jiang T, Levi M
Submitted By
Moshe Levi on 5/2/2011
Status
Published
Journal
Nature reviews. Nephrology
Year
2010
Date Published
6/1/2010
Volume : Pages
6 : 342 - 351
PubMed Reference
20421884
Abstract
Diabetes is the leading cause of end-stage renal disease in developed countries.
In spite of glucose and blood pressure control, for example by use of
angiotensin II receptor blockers, diabetic nephropathy still develops and
progresses in affected patients and the development of additional protective
therapeutic interventions is, therefore, required. Nuclear hormone receptors are
transcription factors that 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 a host of 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. Eight nuclear receptors have
shown a renoprotective effect in the context of diabetic nephropathy. This
Review discusses the evidence regarding the beneficial effects of the activation
of these receptors in preventing the progression of diabetic nephropathy and
describes 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.
Investigators with authorship
Name
Institution
Moshe Levi
Georgetown University
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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