RESUMO
Transient receptor potential (TRP) proteins are components of Ca(2 +) -permeable non-selective cation channels activated by physical and chemical stimulus except for membrane depolarization. The pathophysiological role of TRP channels is documented in heart failure. Especially, canonical TRP subfamily C (TRPC) channels activated by neurohumoral factors have been implicated in the structural remodeling of the heart. TRPC proteins act not only as components of receptor-activated cation channels, but also as protein scaffold to form protein complex with intracellular signaling proteins, leading to amplification of receptor signaling. Recently, selective inhibitors of TRPC channels have been continuously identified, anticipating the possibility of drug discovery targeting TRPC channels for the treatment of heart failure.
