title: Podocytopathy in diabetes: a metabolic and endocrine disorder.
abstract: Diabetic nephropathy (DN) represents a major public health cost. Tight glycemic and blood pressure control can dramatically slow, but not stop, the progression of the disease, and a large number of patients progress toward end-stage renal disease despite currently available interventions. An early and key event in the development of DN is loss of podocyte function (or glomerular visceral epithelial cells) from the kidney glomerulus, where they contribute to the integrity of the glomerular filtration barrier. Recent evidence suggests that podocytes can be the direct target of circulating hormones, lipids, and adipokines that are affected in diabetes. We review the clinical and experimental evidence implicating novel endocrine and metabolic pathways in the pathogenesis of podocyte dysfunction and the development of DN.
authors: Department of Physiology and Biophysics, University of Miami Miller School of Medicine, FL, USA.
authors: Ana
authors: A
authors: Diez-Sampedro
authors: Oliver
authors: O
authors: Lenz
authors: Alessia
authors: A
authors: Fornoni
mesh_terms: D054392:Adipokines / Q000502:physiology; D000328:Adult; D000419:Albuminuria / Q000209:etiology / Q000503:physiopathology; D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000378:metabolism; D003928:Diabetic Nephropathies / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology / Q000517:prevention & control; D006728:Hormones / Q000502:physiology; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007678:Kidney Glomerulus / Q000503:physiopathology / Q000648:ultrastructure; D008297:Male; D051379:Mice; D008954:Models, Biological; D018384:Oxidative Stress; D050199:Podocytes / Q000378:metabolism / Q000473:pathology*; D012084:Renin-Angiotensin System / Q000502:physiology; D014807:Vitamin D / Q000502:physiology
chemical_list: D054392:Adipokines; D006728:Hormones; D007004:Hypoglycemic Agents; D014807:Vitamin D