TRPC6 channels and their binding partners in podocytes: Role in glomerular filtration and pathophysiology

Stuart E. Dryer, Jochen Reiser

Research output: Contribution to journalReview articlepeer-review

127 Scopus citations


Loss or dysfunction of podocytes is a major cause of glomerular kidney disease. Several genetic forms of glomerular disease are caused by mutations in genes that encode structural elements of the slit diaphragm or the underlying cytoskeleton of podocyte foot processes. The recent discovery that gain-of-function mutations in Ca2+-permeable canonical transient receptor potential-6 channels (TRPC6) underlie a subset of familial forms of focal segmental glomerulosclerosis (FSGS) has focused attention on the basic cellular physiology of podocytes. Several recent studies have examined the role of Ca2+ dynamics in normal podocyte function and their possible contributions to glomerular disease. This review summarizes the properties of TRPC6 and related channels, focusing on their permeation and gating properties, the nature of mutations associated with familial FSGS, and the role of TRPC channels in podocyte cell biology as well as in glomerular pathophysiology. TRPC6 interacts with several proteins in podocytes, including essential slit diaphragm proteins and mechanosensitive large-conductance Ca2+- activated K+ channels. The signaling dynamics controlling ion channel function and localization in podocytes appear to be quite complex.

Original languageEnglish (US)
Pages (from-to)F689-F701
JournalAmerican Journal of Physiology - Renal Physiology
Issue number4
StatePublished - Oct 2010
Externally publishedYes


  • Cytoskeleton
  • FSGS
  • Glomerular disease
  • Renal function

ASJC Scopus subject areas

  • Physiology
  • Urology


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