TRPC6 and cardiac hypertrophy: Consistent with the data obtained from TRPC3/C6 ectopic expression model, cardiomyocyte-specific overexpression of dominant negative mutants of TRPC3 or TRPC6 [N-terminal fragment of TRPC3 or pore-dead mutant (L678-W680 replaced to three alanine residues) of TRPC6] suppressed both neurohumoral factor-induced and pressure-overload-induced cardiac hypertrophy and dysfunction (60).