Background The hallmark of podocytopathies, such as FSGS, is podocyte injury resulting in
proteinuria. Transient receptor potential channel C6 (TRPC6) is a calcium-conducting ion
channel expressed at the slit diaphragm. TRPC6 gain-of-function mutations and glomerular
TRPC6 overexpression are associated with proteinuria. However, the pathways linking
TRPC6 to podocyte injury, which is characterized by loss of the slit diaphragm protein
nephrin, activation of several intracellular pathways (including calcineurin-NFAT signaling) …