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Interaction of receptor for advanced glycation end products with advanced oxidation protein products induces podocyte

Yasuhiko Yamamoto1, Hiroshi Yamamoto

  • 1Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan. yasuyama@med.kanazawa-u.ac.jp

Kidney International
|September 15, 2012
PubMed

Insights

Advanced oxidation protein products (AOPPs) and receptor for advanced glycation end products (RAGE) cause kidney podocyte injury. Blocking RAGE may prevent and treat podocyte apoptosis in chronic kidney disease (CKD).

Area of Science:

  • Nephrology
  • Molecular Biology
  • Oxidative Stress Research

Background:

  • Chronic kidney disease (CKD) involves progressive renal function decline.
  • Podocyte injury and loss are key factors in diabetic and nondiabetic CKD pathogenesis.

Purpose of the Study:

  • To investigate the role of advanced oxidation protein products (AOPPs) and their interaction with the receptor for advanced glycation end products (RAGE) in podocyte injury.
  • To evaluate the potential of blocking RAGE as a therapeutic strategy for oxidative stress-induced podocyte apoptosis in CKD.

Main Methods:

  • Utilized cultured podocytes and a mouse model injected with AOPPs.
  • Examined the effects of AOPPs and RAGE interaction on podocyte injury and apoptosis.

Main Results:

  • Demonstrated that the association between AOPPs and RAGE directly elicits podocyte injuries.
  • Confirmed podocyte apoptosis is induced by oxidative stress-related AOPPs.

Conclusions:

  • The interaction of AOPPs with RAGE is a significant contributor to podocyte damage in CKD.
  • Blocking RAGE shows promise as a preventive and therapeutic approach against AOPP-induced podocyte apoptosis in CKD.

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