In the kidney, the receptor for advanced glycation end products (RAGE) is principally
expressed in the podocyte at low levels, but is upregulated in both human and mouse
glomerular diseases. Because podocyte injury is central to proteinuric states, such as the
nephrotic syndrome, the murine adriamycin nephrosis model was used to explore the role of
RAGE in podocyte damage. In this model, administration of the anthracycline antibiotic
adriamycin provokes severe podocyte stress and glomerulosclerosis. In contrast to wild-type …