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dc.contributor.author
Damm, Tatiana Benavides
dc.contributor.author
Egli, Marcel
dc.date.accessioned
2019-09-30T14:42:06Z
dc.date.available
2017-06-11T06:48:52Z
dc.date.available
2019-09-30T14:42:06Z
dc.date.issued
2014
dc.identifier.issn
1015-8987
dc.identifier.issn
1421-9778
dc.identifier.other
10.1159/000356667
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/82403
dc.identifier.doi
10.3929/ethz-b-000082403
dc.description.abstract
Mechanotransduction is a process where cells sense their surroundings and convert the physical forces in their environment into an appropriate response. Calcium plays a crucial role in the translation of such forces to biochemical signals that control various biological processes fundamental in muscle development. The mechanical stimulation of muscle cells may for example result from stretch, electric and magnetic stimulation, shear stress, and altered gravity exposure. The response, mainly involving changes in intracellular calcium concentration then leads to a cascade of events by the activation of downstream signaling pathways. The key calcium-dependent pathways described here include the nuclear factor of activated T cells (NFAT) and mitogen-activated protein kinase (MAPK) activation. The subsequent effects in cellular homeostasis consist of cytoskeletal remodeling, cell cycle progression, growth, differentiation, and apoptosis, all necessary for healthy muscle development, repair, and regeneration. A deregulation from the normal process due to disuse, trauma, or disease can result in a clinical condition such as muscle atrophy, which entails a significant loss of muscle mass. In order to develop therapies against such diseased states, we need to better understand the relevance of calcium signaling and the downstream responses to mechanical forces in skeletal muscle. The purpose of this review is to discuss in detail how diverse mechanical stimuli cause changes in calcium homeostasis by affecting membrane channels and the intracellular stores, which in turn regulate multiple pathways that impart these effects and control the fate of muscle tissue.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Karger
en_US
dc.rights.uri
http://creativecommons.org/licenses/by-nc/3.0/
dc.subject
Mechano-gated calcium channels
en_US
dc.subject
Calcium signaling
en_US
dc.subject
Mechanical forces
en_US
dc.subject
Mechanosensation
en_US
dc.subject
Mechanoresponses
en_US
dc.subject
Muscle atrophy
en_US
dc.subject
Muscle dystrophy
en_US
dc.title
Calcium's Role in Mechanotransduction during Muscle Development
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution-NonCommercial 3.0 Unported
dc.date.published
2014-01-31
ethz.journal.title
Cellular Physiology and Biochemistry
ethz.journal.volume
33
en_US
ethz.journal.issue
2
en_US
ethz.journal.abbreviated
Cell. physiol. biochem.
ethz.pages.start
249
en_US
ethz.pages.end
272
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.nebis
000580750
ethz.publication.place
Basel
en_US
ethz.publication.status
published
en_US
ethz.date.deposited
2017-06-11T06:52:39Z
ethz.source
ECIT
ethz.identifier.importid
imp593651c59d9c669374
ethz.ecitpid
pub:129953
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-20T16:03:28Z
ethz.rosetta.lastUpdated
2020-02-15T21:50:09Z
ethz.rosetta.versionExported
true
ethz.COinS
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