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Updated: Jul 6, 2026

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
RAGE in diabetic nephropathy
Hiroshi Yamamoto1, Takuo Watanabe, Yasuhiko Yamamoto
1Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science, 13-1 Takara-machi, Kanazawa 920-8640, Japan. yamamoto@med.kanazawa-u.ac.jp
Advanced glycation endproducts (AGE) and their receptor (RAGE) drive diabetic nephropathy. Targeting AGE and RAGE pathways offers a promising therapeutic strategy for preventing kidney disease in diabetics.
Area of Science:
- Nephrology
- Diabetology
- Vascular Biology
Background:
- Diabetic nephropathy is a complex condition.
- Advanced glycation endproducts (AGE) contribute to vascular damage in diabetes.
- The receptor for AGE (RAGE) mediates AGE-induced cellular dysfunction.
Purpose of the Study:
- To investigate the role of AGE and RAGE in diabetic nephropathy.
- To evaluate AGE and RAGE as therapeutic targets for diabetic kidney disease.
Main Methods:
- Utilized RAGE-overexpressing and RAGE-deficient mouse models of diabetes.
- Assessed indices of nephropathy in diabetic conditions.
- Investigated the effects of inhibiting AGE formation.
Main Results:
- RAGE overexpression exacerbated diabetic nephropathy.
- Inhibiting AGE formation prevented nephropathy exacerbation in diabetic mice.
- RAGE deficiency ameliorated diabetic nephropathy.
Conclusions:
- AGE and RAGE are key contributors to diabetic nephropathy.
- Targeting AGE formation and RAGE signaling presents a viable therapeutic approach for diabetic kidney disease.
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