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Myostatin and the skeletal muscle atrophy and hypertrophy signaling pathways
- Source :
- Cellular and Molecular Life Sciences, Cellular and Molecular Life Sciences, Springer Verlag, 2014, 71 (22), pp.4361-4371. ⟨10.1007/s00018-014-1689-x⟩, Cellular and Molecular Life Sciences, Springer Verlag, 2014, 71 (22), pp.4361-4371. 〈10.1007/s00018-014-1689-x〉
- Publication Year :
- 2014
- Publisher :
- HAL CCSD, 2014.
-
Abstract
- Myostatin, a member of the transforming growth factor-β superfamily, is a potent negative regulator of skeletal muscle growth and is conserved in many species, from rodents to humans. Myostatin inactivation can induce skeletal muscle hypertrophy, while its overexpression or systemic administration causes muscle atrophy. As it represents a potential target for stimulating muscle growth and/or preventing muscle wasting, myostatin regulation and functions in the control of muscle mass have been extensively studied. A wealth of data strongly suggests that alterations in skeletal muscle mass are associated with dysregulation in myostatin expression. Moreover, myostatin plays a central role in integrating/mediating anabolic and catabolic responses. Myostatin negatively regulates the activity of the Akt pathway, which promotes protein synthesis, and increases the activity of the ubiquitin-proteasome system to induce atrophy. Several new studies have brought new information on how myostatin may affect both ribosomal biogenesis and translation efficiency of specific mRNA subclasses. In addition, although myostatin has been identified as a modulator of the major catabolic pathways, including the ubiquitin-proteasome and the autophagy-lysosome systems, the underlying mechanisms are only partially understood. The goal of this review is to highlight outstanding questions about myostatin-mediated regulation of the anabolic and catabolic signaling pathways in skeletal muscle. Particular emphasis has been placed on (1) the cross-regulation between myostatin, the growth-promoting pathways and the proteolytic systems; (2) how myostatin inhibition leads to muscle hypertrophy; and (3) the regulation of translation by myostatin.
- Subjects :
- medicine.medical_specialty
muscle differentiation
Myostatin
Protein degradation
[ SDV.BA ] Life Sciences [q-bio]/Animal biology
growth differentiation factor-8
Muscle hypertrophy
03 medical and health sciences
Cellular and Molecular Neuroscience
0302 clinical medicine
Internal medicine
Myokine
medicine
Humans
[ SDV.BDD ] Life Sciences [q-bio]/Development Biology
Muscle, Skeletal
Molecular Biology
[SDV.BDD]Life Sciences [q-bio]/Development Biology
PI3K/AKT/mTOR pathway
Cell Proliferation
030304 developmental biology
Pharmacology
0303 health sciences
biology
TOR Serine-Threonine Kinases
[SDV.BA]Life Sciences [q-bio]/Animal biology
Skeletal muscle
Cell Differentiation
muscle homeostasis
Hypertrophy
Cell Biology
musculoskeletal system
Muscle atrophy
Muscular Atrophy
Endocrinology
medicine.anatomical_structure
GDF11
biology.protein
protein degradation
translational machinery
mTOR
Molecular Medicine
medicine.symptom
030217 neurology & neurosurgery
Signal Transduction
Subjects
Details
- Language :
- English
- ISSN :
- 1420682X and 14209071
- Database :
- OpenAIRE
- Journal :
- Cellular and Molecular Life Sciences, Cellular and Molecular Life Sciences, Springer Verlag, 2014, 71 (22), pp.4361-4371. ⟨10.1007/s00018-014-1689-x⟩, Cellular and Molecular Life Sciences, Springer Verlag, 2014, 71 (22), pp.4361-4371. 〈10.1007/s00018-014-1689-x〉
- Accession number :
- edsair.doi.dedup.....139405178bdefe80f00ced685abcd9b5