Podocyte dysfunction, one of the major causes of proteinuria, leads to glomerulosclerosis
and end stage renal disease, but its underlying mechanism remains poorly understood.
Here we show that Wnt/β-catenin signaling plays a critical role in podocyte injury and
proteinuria. Treatment with adriamycin induced Wnt and activated β-catenin in mouse
podocytes. Overexpression of Wnt1 in vivo activated glomerular β-catenin and aggravated
albuminuria and adriamycin-induced suppression of nephrin expression, whereas blockade …