TRPC6 and glomerular disorder: Since TRPC6 is overexpressed in several human glomerular diseases and animal models of podocyte injury and glomerular disease, it could be a common effector in the resulting podocyte injury.[13], [17] We have previously shown that AngII-mediated activation of the deleterious calcineurin/NFAT pathway, which includes Ca2+ influx through TRPC6 itself, leads to enhanced transcriptional expression of TRPC6 in the podocyte.