Abstract:

ABSTRACT Podocytes express canonical transient receptor potential-6 (TRPC6 ), which is a nonselective, Ca(2+)-permeable, cationic channel. Increasing evidence indicates that TRPC6 is involved in AII-induced podocyte injury through pathological calcium signaling in glomerular pathophysiology. This study summarizes the properties of TRPC6 and the signal transmission mechanisms of TRPC6-mediated and AII -induced podocyte injury.

Key words: TRPC6, Ca2+, Angiotensin II, podocyte injury, transmission mechanisms