The general mechanism for this is that the continued hyperactivation of podocyte TRPC6 channels results in [Ca2+] ion overload, which can be activated in response to G protein signaling specifically via a diacylglycerol-dependent pathway, and then induces foot process effacement, podocyte detachment, and glomerulosclerosis [15, 17, 18]. This evidence concerns the gene TRPC6 and glomerulosclerosis.