Chapter title |
Neurological and Motor Disorders: TRPC in the Skeletal Muscle
|
---|---|
Chapter number | 28 |
Book title |
Store-Operated Ca²⁺ Entry (SOCE) Pathways
|
Published in |
Advances in experimental medicine and biology, January 2017
|
DOI | 10.1007/978-3-319-57732-6_28 |
Pubmed ID | |
Book ISBNs |
978-3-31-957731-9, 978-3-31-957732-6
|
Authors |
Sophie Saüc, Maud Frieden |
Abstract |
Transient receptor potential canonical (TRPC) channels belong to the large family of TRPs that are mostly nonselective cation channels with a great variety of gating mechanisms. TRPC are composed of seven members that can all be activated downstream of agonist-induced phospholipase C stimulation, but some members are also stretch-activated and/or are part of the store-operated Ca(2+) entry (SOCE) pathway. Skeletal muscles generate contraction via an explosive increase of cytosolic Ca(2+) concentration resulting almost exclusively from sarcoplasmic reticulum Ca(2+) channel opening. Even if neglected for a long time, it is now commonly accepted that Ca(2+) entry via SOCE and other routes is essential to sustain contractions of the skeletal muscle. In addition, Ca(2+) influx is required during muscle regeneration, and alteration of the influx is associated with myopathies. In this chapter, we review the implication of TRPC channels at different stages of muscle regeneration, in adult muscle fibers, and discuss their implication in myopathies. |
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