Hiroyuki Watanabe, Kenji Iino, Takayoshi Ohba and Hiroshi Ito Pages 283 - 294 ( 12 )
Over the past 20 years, studies of transient receptor potential (TRP) channels have significantly extended our knowledge regarding the molecular basis of Ca2+ signals in cardiac myocytes. The functional significance of cardiac TRP channels is likely connected to the alteration of membrane potential or Ca2+ entry into a noncontractile compartment, where gene expression responsible for various cardiac diseases is induced. This review highlights some aspects of TRP channels with anticipated roles in cardiac disease. Evidence suggests that (a) increased activities of TRPC1, TRPC3, or TRPC6 are involved in the development of cardiac hypertrophy, where these TRPC channels act as unique sensors for a wide range of hypertrophic stimuli, and (b) mutations in TRPM4 are now recognized as causes of human cardiac conduction disorders. Ultimately, TRP channels may become novel pharmacological targets in the treatment of human cardiac disease.
Cardiac arrhythmia, cardiac hypertrophy, Orai1, Stim1, TRPC1, TRPC3, TRPC6, TRPM4
Department of Cardiovascular and Respiratory Medicine, Akita University Graduate School of Medicine, Hondoh 1-1-1, Akita 010-8543, Japan.