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RAGE mediates podocyte injury in adriamycin-induced glomerulosclerosis

Jiancheng Guo1, Radha Ananthakrishnan, Wu Qu

  • 1Department of Surgery, Columbia University Medical Center, New York, New York 10025, USA.

Journal of the American Society of Nephrology : JASN
|February 8, 2008
PubMed

Insights

The receptor for advanced glycation end products (RAGE) exacerbates kidney podocyte injury and glomerulosclerosis. Blocking RAGE protects against adriamycin-induced nephropathy, suggesting RAGE as a therapeutic target for proteinuric kidney diseases.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pathology

Background:

  • Receptor for advanced glycation end products (RAGE) is upregulated in kidney glomerular diseases.
  • Podocyte injury is central to proteinuric conditions like nephrotic syndrome.

Purpose of the Study:

  • To investigate the role of RAGE in adriamycin-induced podocyte damage and glomerulosclerosis in a murine model.

Main Methods:

  • Utilized the adriamycin nephrosis model in wild-type and RAGE-null mice.
  • Assessed podocyte foot process effacement, albuminuria, and glomerulosclerosis.
  • Investigated RAGE ligand generation and the effect of soluble RAGE treatment.
  • Performed in vitro studies on cultured murine podocytes exposed to adriamycin and RAGE ligands.

Main Results:

  • RAGE-null mice showed significant protection against adriamycin-induced podocyte injury, albuminuria, and glomerulosclerosis.
  • Adriamycin treatment rapidly generated RAGE ligands; soluble RAGE administration mitigated podocyte damage.
  • In vitro, adriamycin induced advanced glycation end product (AGE) formation and RAGE ligand activation of NADPH-oxidase and pro-fibrotic factors in podocytes.

Conclusions:

  • RAGE signaling contributes to podocyte injury and glomerulosclerosis in experimental nephropathy.
  • Targeting RAGE may offer a therapeutic strategy for proteinuric kidney diseases, including focal segmental glomerulosclerosis.

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