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RAGE and the pathogenesis of chronic kidney disease

Vivette D'Agati1, Ann Marie Schmidt

  • 1Department of Pathology, Columbia University Medical Center, New York, NY 10032, USA.

Nature Reviews. Nephrology
|April 28, 2010
PubMed

Insights

The receptor for advanced glycation endproducts (RAGE) plays a key role in kidney disease beyond diabetes. Targeting RAGE may offer a new treatment strategy for chronic kidney disease.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • The receptor for advanced glycation endproducts (RAGE) is a multiligand signal transduction receptor.
  • RAGE binds various ligands including advanced glycation endproducts, S100 proteins, HMGB1, advanced oxidation protein products, and amyloid fibrils.
  • While initially studied in diabetic nephropathy, RAGE is implicated in other kidney diseases.

Purpose of the Study:

  • To explore the role of RAGE in the pathogenesis of non-diabetic renal disorders.
  • To investigate the potential of RAGE antagonism as a therapeutic strategy for chronic kidney disease.

Main Methods:

  • Review of existing literature and experimental data.
  • Analysis of studies using transgenic mouse models with altered RAGE expression or function.
  • Examination of research involving pharmacological blockade or genetic deletion/modification of RAGE.

Main Results:

  • RAGE is involved in the pathogenesis of obesity-related glomerulopathy, doxorubicin-induced nephropathy, hypertensive nephropathy, lupus nephritis, renal amyloidosis, and ischemic renal injuries.
  • Modulation of RAGE expression or function impacts the functional and pathological characteristics of these nephropathies.
  • Evidence suggests a significant link between RAGE and the development of various kidney diseases.

Conclusions:

  • RAGE is a critical factor in the development of diverse nephropathies, not limited to diabetic kidney disease.
  • Antagonism of RAGE presents a promising therapeutic avenue for managing chronic kidney disease.

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