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Updated: Jun 20, 2026

An Efficient Sieving Method to Isolate Intact Glomeruli from Adult Rat Kidney
Published on: November 1, 2018
RAGE, glomerulosclerosis and proteinuria: roles in podocytes and endothelial cells
Vivette D'Agati1, Shi Fang Yan, Ravichandran Ramasamy
1Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Abstract:
The multi-ligand Receptor for Advanced Glycation Endproducts (RAGE) is expressed in podocytes and endothelial cells in the human and murine glomerulus. Although present at low levels in homeostasis, RAGE expression is increased during disease. Pharmacological antagonism of RAGE or its genetic deletion imparts marked protection from podocyte effacement, albuminuria and glomerular sclerosis in disease models. In human subjects, associations between specific genetic polymorphisms of RAGE and levels of soluble forms of RAGE are linked to disease states in the kidney. In this review, we summarize the evidence from mouse to man, linking RAGE to the pathogenesis of nephropathy.
Insights
The Receptor for Advanced Glycation Endproducts (RAGE) plays a key role in kidney disease. Blocking RAGE offers protection against nephropathy in various models, highlighting its therapeutic potential.
Area of Science:
- Nephrology
- Molecular Biology
- Immunology
Background:
- Receptor for Advanced Glycation Endproducts (RAGE) is expressed in glomerular podocytes and endothelial cells.
- RAGE levels increase during kidney disease, suggesting a role in pathogenesis.
- Genetic variations in RAGE are associated with kidney disease states in humans.
Purpose of the Study:
- To review the evidence linking RAGE to the development of nephropathy.
- To summarize findings from both animal models and human studies.
Main Methods:
- Review of existing literature on RAGE in kidney disease.
- Analysis of studies involving RAGE antagonism or genetic deletion in disease models.
- Examination of human genetic association studies.
Main Results:
- Pharmacological inhibition or genetic deletion of RAGE significantly protects against podocyte damage, albuminuria, and glomerulosclerosis in experimental models.
- Increased RAGE expression is observed in diseased kidneys.
- Genetic polymorphisms of RAGE and levels of soluble RAGE correlate with kidney disease severity in humans.
Conclusions:
- RAGE is implicated in the pathogenesis of various forms of nephropathy.
- Targeting RAGE presents a potential therapeutic strategy for kidney diseases.
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