Journal
CELLS
Volume 9, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/cells9040850
Keywords
skeletal muscle; TRPC; Ca2+ entry; SOCE; Duchenne muscular dystrophy
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Funding
- Mid-career Researcher Program through National Research Foundation of Korea grant [NRF-2019R1A2C1086858]
- National Institute of Arthritis and Musculoskeletal and Skin Diseases grant [1R01AR068897-01A1]
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Ca2+ itself or Ca2+-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 Ca2+ is required for coordinated Ca2+-dependent skeletal muscle functions, such as the interactions of contractile proteins during contraction. Intracellular Ca2+ movements between the cytosol and sarcoplasmic reticulum (SR) are strictly regulated to maintain the appropriate Ca2+ supply in skeletal muscle cells. Added to intracellular Ca2+ movements, the contribution of extracellular Ca2+ 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 Ca2+ 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 Ca2+ entry (SOCE) channels under normal conditions and the potential abnormal properties of TRPCs in muscle diseases such as Duchenne muscular dystrophy (DMD).
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