Neurological and Motor Disorders: TRPC in the Skeletal Muscle

Adv Exp Med Biol. 2017:993:557-575. doi: 10.1007/978-3-319-57732-6_28.

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 Ca2+ entry (SOCE) pathway. Skeletal muscles generate contraction via an explosive increase of cytosolic Ca2+ concentration resulting almost exclusively from sarcoplasmic reticulum Ca2+ channel opening. Even if neglected for a long time, it is now commonly accepted that Ca2+ entry via SOCE and other routes is essential to sustain contractions of the skeletal muscle. In addition, Ca2+ 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.

Keywords: Calcium entry; Muscle regeneration; Myopathies; Skeletal muscle; TRPC.

Publication types

  • Review

MeSH terms

  • Animals
  • Calcium / metabolism
  • Calcium Signaling / physiology
  • Humans
  • Motor Disorders / metabolism*
  • Muscle Fibers, Skeletal / metabolism*
  • Nervous System Diseases / metabolism*
  • Sarcoplasmic Reticulum / metabolism
  • TRPC Cation Channels / metabolism*

Substances

  • TRPC Cation Channels
  • Calcium