Phosphoinositides in Ca2+ signaling and excitation–contraction coupling in skeletal muscle: an old player and newcomers

L. Csernoch, Vincent Jacquemond

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Since the postulate, 30 years ago, that phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) as the precursor of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) would be critical for skeletal muscle excitation–contraction (EC) coupling, the issue of whether phosphoinositides (PtdInsPs) may have something to do with Ca2+ signaling in muscle raised limited interest, if any. In recent years however, the PtdInsP world has expanded considerably with new functions for PtdIns(4,5)P2 but also with functions for the other members of the PtdInsP family. In this context, the discovery that genetic deficiency in a PtdInsP phosphatase has dramatic consequences on Ca2+ homeostasis in skeletal muscle came unanticipated and opened up new perspectives in regards to how PtdInsPs modulate muscle Ca2+ signaling under normal and disease conditions. This review intends to make an update of the established, the questioned, and the unknown regarding the role of PtdInsPs in skeletal muscle Ca2+ homeostasis and EC coupling, with very specific emphasis given to Ca2+ signals in differentiated skeletal muscle fibers.

Original languageEnglish
JournalJournal of Muscle Research and Cell Motility
DOIs
Publication statusAccepted/In press - Sep 16 2015

Fingerprint

Phosphatidylinositol 4,5-Diphosphate
Phosphatidylinositols
Muscle
Skeletal Muscle
Homeostasis
Muscles
Inositol 1,4,5-Trisphosphate
Skeletal Muscle Fibers
Phosphoric Monoester Hydrolases
Fibers

Keywords

  • Calcium homeostasis
  • Excitation–contraction coupling
  • Phosphoinositide
  • Ryanodine receptor
  • Sarcoplasmic reticulum Ca<sup>2+</sup> release
  • Skeletal muscle fibers

ASJC Scopus subject areas

  • Physiology
  • Cell Biology
  • Biochemistry

Cite this

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abstract = "Since the postulate, 30 years ago, that phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) as the precursor of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) would be critical for skeletal muscle excitation–contraction (EC) coupling, the issue of whether phosphoinositides (PtdInsPs) may have something to do with Ca2+ signaling in muscle raised limited interest, if any. In recent years however, the PtdInsP world has expanded considerably with new functions for PtdIns(4,5)P2 but also with functions for the other members of the PtdInsP family. In this context, the discovery that genetic deficiency in a PtdInsP phosphatase has dramatic consequences on Ca2+ homeostasis in skeletal muscle came unanticipated and opened up new perspectives in regards to how PtdInsPs modulate muscle Ca2+ signaling under normal and disease conditions. This review intends to make an update of the established, the questioned, and the unknown regarding the role of PtdInsPs in skeletal muscle Ca2+ homeostasis and EC coupling, with very specific emphasis given to Ca2+ signals in differentiated skeletal muscle fibers.",
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