Skeletal muscle Ca2+ mishandling: Another effect of bone-to-muscle signaling

Jenna N. Regan, David Waning, Theresa A. Guise

Research output: Contribution to journalReview article

6 Citations (Scopus)

Abstract

Our appreciation of crosstalk between muscle and bone has recently expanded beyond mechanical force-driven events to encompass a variety of signaling factors originating in one tissue and communicating to the other. While the recent identification of new 'myokines' has shifted some focus to the role of muscle in this partnership, bone-derived factors and their effects on skeletal muscle should not be overlooked. This review summarizes some previously known mediators of bone-to-muscle signaling and also recent work identifying a new role for bone-derived TGF-β as a cause of skeletal muscle weakness in the setting of cancer-induced bone destruction. Oxidation of the ryanodine receptor/calcium release channel (RyR1) in skeletal muscle occurs via a TGF-β-Nox4-RyR1 axis and leads to calcium mishandling and decreased muscle function. Multiple points of potential therapeutic intervention were identified, from preventing the bone destruction to stabilizing the RYR1 calcium channel. This new data reinforces the concept that bone can be an important source of signaling factors in pathphysiological settings.

Original languageEnglish (US)
Pages (from-to)24-29
Number of pages6
JournalSeminars in Cell and Developmental Biology
Volume49
DOIs
StatePublished - Jan 1 2016

Fingerprint

Skeletal Muscle
Bone and Bones
Muscles
Ryanodine Receptor Calcium Release Channel
Bone Neoplasms
Muscle Weakness
Calcium Channels
Calcium
Therapeutics

All Science Journal Classification (ASJC) codes

  • Developmental Biology
  • Cell Biology

Cite this

@article{8e0f2ef307e444a68d2064191543e8b9,
title = "Skeletal muscle Ca2+ mishandling: Another effect of bone-to-muscle signaling",
abstract = "Our appreciation of crosstalk between muscle and bone has recently expanded beyond mechanical force-driven events to encompass a variety of signaling factors originating in one tissue and communicating to the other. While the recent identification of new 'myokines' has shifted some focus to the role of muscle in this partnership, bone-derived factors and their effects on skeletal muscle should not be overlooked. This review summarizes some previously known mediators of bone-to-muscle signaling and also recent work identifying a new role for bone-derived TGF-β as a cause of skeletal muscle weakness in the setting of cancer-induced bone destruction. Oxidation of the ryanodine receptor/calcium release channel (RyR1) in skeletal muscle occurs via a TGF-β-Nox4-RyR1 axis and leads to calcium mishandling and decreased muscle function. Multiple points of potential therapeutic intervention were identified, from preventing the bone destruction to stabilizing the RYR1 calcium channel. This new data reinforces the concept that bone can be an important source of signaling factors in pathphysiological settings.",
author = "Regan, {Jenna N.} and David Waning and Guise, {Theresa A.}",
year = "2016",
month = "1",
day = "1",
doi = "10.1016/j.semcdb.2015.11.007",
language = "English (US)",
volume = "49",
pages = "24--29",
journal = "Seminars in Cell and Developmental Biology",
issn = "1084-9521",
publisher = "Academic Press Inc.",

}

Skeletal muscle Ca2+ mishandling : Another effect of bone-to-muscle signaling. / Regan, Jenna N.; Waning, David; Guise, Theresa A.

In: Seminars in Cell and Developmental Biology, Vol. 49, 01.01.2016, p. 24-29.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Skeletal muscle Ca2+ mishandling

T2 - Another effect of bone-to-muscle signaling

AU - Regan, Jenna N.

AU - Waning, David

AU - Guise, Theresa A.

PY - 2016/1/1

Y1 - 2016/1/1

N2 - Our appreciation of crosstalk between muscle and bone has recently expanded beyond mechanical force-driven events to encompass a variety of signaling factors originating in one tissue and communicating to the other. While the recent identification of new 'myokines' has shifted some focus to the role of muscle in this partnership, bone-derived factors and their effects on skeletal muscle should not be overlooked. This review summarizes some previously known mediators of bone-to-muscle signaling and also recent work identifying a new role for bone-derived TGF-β as a cause of skeletal muscle weakness in the setting of cancer-induced bone destruction. Oxidation of the ryanodine receptor/calcium release channel (RyR1) in skeletal muscle occurs via a TGF-β-Nox4-RyR1 axis and leads to calcium mishandling and decreased muscle function. Multiple points of potential therapeutic intervention were identified, from preventing the bone destruction to stabilizing the RYR1 calcium channel. This new data reinforces the concept that bone can be an important source of signaling factors in pathphysiological settings.

AB - Our appreciation of crosstalk between muscle and bone has recently expanded beyond mechanical force-driven events to encompass a variety of signaling factors originating in one tissue and communicating to the other. While the recent identification of new 'myokines' has shifted some focus to the role of muscle in this partnership, bone-derived factors and their effects on skeletal muscle should not be overlooked. This review summarizes some previously known mediators of bone-to-muscle signaling and also recent work identifying a new role for bone-derived TGF-β as a cause of skeletal muscle weakness in the setting of cancer-induced bone destruction. Oxidation of the ryanodine receptor/calcium release channel (RyR1) in skeletal muscle occurs via a TGF-β-Nox4-RyR1 axis and leads to calcium mishandling and decreased muscle function. Multiple points of potential therapeutic intervention were identified, from preventing the bone destruction to stabilizing the RYR1 calcium channel. This new data reinforces the concept that bone can be an important source of signaling factors in pathphysiological settings.

UR - http://www.scopus.com/inward/record.url?scp=84958624000&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84958624000&partnerID=8YFLogxK

U2 - 10.1016/j.semcdb.2015.11.007

DO - 10.1016/j.semcdb.2015.11.007

M3 - Review article

C2 - 26593325

AN - SCOPUS:84958624000

VL - 49

SP - 24

EP - 29

JO - Seminars in Cell and Developmental Biology

JF - Seminars in Cell and Developmental Biology

SN - 1084-9521

ER -