TRPCs: Influential Mediators in Skeletal Muscle

Ca(2+) itself or Ca(2+)-dependent signaling pathways play fundamental roles in various cellular processes from cell growth to death. The most representative example can be found in skeletal muscle cells where a well-timed and adequate supply of Ca(2+) is required for coordinated Ca(2+)-dependent skeletal muscle functions, such as the interactions of contractile proteins during contraction. Intracellular Ca(2+) movements between the cytosol and sarcoplasmic reticulum (SR) are strictly regulated to maintain the appropriate Ca(2+) supply in skeletal muscle cells. Added to intracellular Ca(2+) movements, the contribution of extracellular Ca(2+) entry to skeletal muscle functions and its significance have been continuously studied since the early 1990s. Here, studies on the roles of channel proteins that mediate extracellular Ca(2+) entry into skeletal muscle cells using skeletal myoblasts, myotubes, fibers, tissue, or skeletal muscle-originated cell lines are reviewed with special attention to the proposed functions of transient receptor potential canonical proteins (TRPCs) as store-operated Ca(2+) entry (SOCE) channels under normal conditions and the potential abnormal properties of TRPCs in muscle diseases such as Duchenne muscular dystrophy (DMD).