title: Nuclear hormone receptors in diabetic nephropathy.
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.
authors.affiliation: Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Denver, Aurora, CO 80045, USA.
authors.forename: Xiaoxin X
authors.initials: XX
authors.lastname: Wang
authors.forename: Tao
authors.initials: T
authors.lastname: Jiang
authors.forename: Moshe
authors.initials: M
authors.lastname: Levi
mesh_terms: D000818:Animals; D002986:Clinical Trials as Topic; D003928:Diabetic Nephropathies / Q000188:drug therapy* / Q000503:physiopathology*; D018450:Disease Progression; D006360:Heat-Shock Proteins / Q000187:drug effects / Q000502:physiology; D051557:Hepatocyte Nuclear Factor 4 / Q000187:drug effects / Q000502:physiology; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D007555:Isoxazoles / Q000627:therapeutic use; D000071518:Liver X Receptors; D057093:Orphan Nuclear Receptors / Q000187:drug effects / Q000502:physiology; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D018167:Receptors, Calcitriol / Q000187:drug effects / Q000502:physiology; D018160:Receptors, Cytoplasmic and Nuclear / Q000187:drug effects* / Q000502:physiology*; D011960:Receptors, Estrogen / Q000187:drug effects / Q000502:physiology; D045162:Thiazolidinediones / Q000627:therapeutic use; D014157:Transcription Factors / Q000187:drug effects / Q000502:physiology; D014807:Vitamin D / Q000627:therapeutic use; D000099150:Receptor, Farnesoid X-Activated
chemical_list: D006360:Heat-Shock Proteins; D051557:Hepatocyte Nuclear Factor 4; D000960:Hypolipidemic Agents; D007555:Isoxazoles; D000071518:Liver X Receptors; D057093:Orphan Nuclear Receptors; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D018167:Receptors, Calcitriol; D018160:Receptors, Cytoplasmic and Nuclear; D011960:Receptors, Estrogen; D045162:Thiazolidinediones; D014157:Transcription Factors; D014807:Vitamin D; D000099150:Receptor, Farnesoid X-Activated; C486497:PPARGC1A protein, human; C412815:GW 4064