Gain-of-function mutations in the calcium channel TRPC6 lead to autosomal dominant focal
segmental glomerulosclerosis and podocyte expression of TRPC6 is increased in some
acquired human glomerular diseases, particularly in membranous nephropathy. These
observations led to the hypothesis that TRPC6 overactivation is deleterious to podocytes
through pathological calcium signaling, both in genetic and acquired diseases. Here, we
show that the effects of TRPC6 on podocyte function are context-dependent. Overexpression …