title: Receptor for advanced glycation endproducts and progressive kidney disease.
abstract: OBJECTIVE
  Receptor for advanced glycation endproducts (RAGE) is a multiligand receptor of the immunoglobulin superfamily, which binds not only to advanced glycation endproducts, but also to high-mobility group box-1, S100/calgranulins, amyloid fibrils, and lipopolysaccharide. We discuss the pathophysiological role of RAGE in both diabetic and nondiabetic progressive renal diseases, and its potential use for therapeutic interventions in these devastating disorders.
  
  
  RESULTS
  Although initial studies about RAGE focused on diabetic nephropathy, a number of recent findings have revealed that RAGE also actively participates in the pathogenesis of nondiabetic progressive renal diseases, including hypertensive nephropathy, obesity-related glomerulopathy, lupus nephritis, autosomal dominant polycystic kidney disease, renal amyloidosis, and septic acute kidney injury. Furthermore, blocking the RAGE by a neutralizing antibody or genetic deletion of RAGE was found to prevent the development and progression of various renal disorders.
  
  
  CONCLUSIONS
  The interaction of several RAGE ligands with RAGE plays a role in a broad range of progressive kidney diseases. The blockade of the various RAGE ligands-RAGE interactions might be a novel therapeutic strategy for preventing the development and progression of numerous progressive kidney diseases.
authors.affiliation: aDivision of Nephrology, Department of Medicine bDepartment of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume, Fukuoka, Japan *Kei Fukami and Kensei Taguchi contributed equally to the writing of this article.
authors.forename: Kei
authors.initials: K
authors.lastname: Fukami
authors.forename: Kensei
authors.initials: K
authors.lastname: Taguchi
authors.forename: Sho-ichi
authors.initials: S
authors.lastname: Yamagishi
authors.forename: Seiya
authors.initials: S
authors.lastname: Okuda
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000378:metabolism; D000818:Animals; D003928:Diabetic Nephropathies / Q000378:metabolism; D006801:Humans; D006977:Hypertension, Renal / Q000378:metabolism; D007674:Kidney Diseases / Q000378:metabolism*; D008024:Ligands; D008181:Lupus Nephritis / Q000378:metabolism; D009393:Nephritis / Q000378:metabolism; D009765:Obesity / Q000150:complications; D016891:Polycystic Kidney, Autosomal Dominant / Q000378:metabolism; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism*; D051436:Renal Insufficiency, Chronic / Q000209:etiology / Q000378:metabolism; D018805:Sepsis / Q000150:complications
chemical_list: D008024:Ligands; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic