Nuclear hormone receptors in diabetic nephropathy

Nat Rev Nephrol. 2010 Jun;6(6):342-51. doi: 10.1038/nrneph.2010.56. Epub 2010 Apr 27.

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Clinical Trials as Topic
  • Diabetic Nephropathies / drug therapy*
  • Diabetic Nephropathies / physiopathology*
  • Disease Progression
  • Heat-Shock Proteins / drug effects
  • Heat-Shock Proteins / physiology
  • Hepatocyte Nuclear Factor 4 / drug effects
  • Hepatocyte Nuclear Factor 4 / physiology
  • Humans
  • Hypolipidemic Agents / therapeutic use
  • Isoxazoles / therapeutic use
  • Liver X Receptors
  • Orphan Nuclear Receptors / drug effects
  • Orphan Nuclear Receptors / physiology
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Receptors, Calcitriol / drug effects
  • Receptors, Calcitriol / physiology
  • Receptors, Cytoplasmic and Nuclear / drug effects*
  • Receptors, Cytoplasmic and Nuclear / physiology*
  • Receptors, Estrogen / drug effects
  • Receptors, Estrogen / physiology
  • Thiazolidinediones / therapeutic use
  • Transcription Factors / drug effects
  • Transcription Factors / physiology
  • Vitamin D / therapeutic use

Substances

  • Heat-Shock Proteins
  • Hepatocyte Nuclear Factor 4
  • Hypolipidemic Agents
  • Isoxazoles
  • Liver X Receptors
  • Orphan Nuclear Receptors
  • PPARGC1A protein, human
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Receptors, Calcitriol
  • Receptors, Cytoplasmic and Nuclear
  • Receptors, Estrogen
  • Thiazolidinediones
  • Transcription Factors
  • farnesoid X-activated receptor
  • Vitamin D
  • GW 4064