title: TRPC6 in glomerular health and disease: what we know and what we believe.
abstract: Mutations in TRPC6, a member of the transient receptor potential (TRP) superfamily of non-selective cation channels, have been identified as causing a familial form of focal segmental glomerulosclerosis, a disease characterized by proteinuria and progressive renal failure. Here we review the effect of disease-associated mutations on TRPC6 function and place TRPC6 within the context of other proteins central to glomerular and podocyte function. Finally, the known roles of TRPC6 in the kidney and other organ systems are used as a framework to discuss possible signaling pathways that TRPC6 may modulate during normal glomerular function and in disease states.
authors.affiliation: Renal Division, Brigham and Women's Hospital/Harvard Medical School, Boston, MA 02115, USA.
authors.forename: Johannes S
authors.initials: JS
authors.lastname: Schlöndorff
authors.forename: Martin R
authors.initials: MR
authors.lastname: Pollak
mesh_terms: D000818:Animals; D006801:Humans; D007674:Kidney Diseases / Q000378:metabolism* / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000378:metabolism* / Q000502:physiology / Q000503:physiopathology*; D050052:TRPC Cation Channels / Q000502:physiology*; D000074287:TRPC6 Cation Channel
chemical_list: D050052:TRPC Cation Channels; D000074287:TRPC6 Cation Channel; C117032:TRPC6 protein, human; C492146:Trpc6 protein, mouse; C492145:Trpc6 protein, rat