The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Mitochondrial signaling contributes to disuse muscle atrophy
Open accessAbstract
It is well established that long durations of bed rest, limb immobilization, or reduced activity in respiratory muscles during mechanical ventilation results in skeletal muscle atrophy in humans and other animals. The idea that mitochondrial damage/dysfunction contributes to disuse muscle atrophy originated over 40 years ago. These early studies were largely descriptive and did not provide unequivocal evidence that mitochondria play a primary role in disuse muscle atrophy. However, recent experiments have provided direct evidence connecting mitochondrial dysfunction to muscle atrophy. Numerous studies have described changes in mitochondria shape, number, and function in skeletal muscles exposed to prolonged periods of inactivity. Furthermore, recent evidence indicates that increased mitochondrial ROS production plays a key signaling role in both immobilization-induced limb muscle atrophy and diaphragmatic atrophy occurring during prolonged mechanical ventilation. Moreover, new evidence reveals that, during denervation-induced muscle atrophy, increased mitochondrial fragmentation due to fission is a required signaling event that activates the AMPK-FoxO3 signaling axis, which induces the expression of atrophy genes, protein breakdown, and ultimately muscle atrophy. Collectively, these findings highlight the importance of future research to better understand the mitochondrial signaling mechanisms that contribute to disuse muscle atrophy and to develop novel therapeutic interventions for prevention of inactivity-induced skeletal muscle atrophy.
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Cites
Identification of ubiquitin ligases required for skeletal muscle atrophy.
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“For example, in muscle fibers, mitochondria play an important role in the regulation of myonuclear apoptosis and also serve as a sink for calcium (40).”
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“Hence, in animals, the loss of skeletal muscle protein that occurs during inactivity is due to a decline in protein synthesis and increased protein breakdown with accelerated proteolysis playing the dominant role (24, 58, 59).”
BackgroundMitochondrial damage induced by conditions of oxidative stress
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Mitochondrial fission and remodelling contributes to muscle atrophy
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Mechanisms of disuse muscle atrophy: role of oxidative stress
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Self-citation
Cited by
Maintenance of Skeletal Muscle Mitochondria in Health, Exercise, and Aging
Hood, D. A., Memme, J. M., Oliveira, A. N., & Triolo, M. (2019) · Annual Review of Physiology · doi:10.1146/annurev-physiol-020518-114310 · Cited by 567
Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy
Calvani, R., Joseph, A.-M., Adhihetty, P. J., Miccheli, A., Bossola, M., Leeuwenburgh, C., Bernabei, R., & Marzetti, E. (2013) · bchm · doi:10.1515/hsz-2012-0247 · Cited by 328
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Self-citationPhysical Exercise in the Oldest Old
Valenzuela, P. L., Castillo‐García, A., Morales, J. S., Izquierdo, M., Serra‐Rexach, J. A., Santos‐Lozano, A., & Lucia, A. (2019) · Comprehensive Physiology · doi:10.1002/cphy.c190002 · Cited by 152
McGlory, C., von Allmen, M. T., Stokes, T., Morton, R. W., Hector, A. J., Lago, B. A., Raphenya, A. R., Smith, B. K., McArthur, A. G., Steinberg, G. R., et al. (2018) · The Journals of Gerontology: Series A · doi:10.1093/gerona/glx203 · Cited by 113
Metadata
- Authors
- Powers, S. K., Wiggs, M. P., Duarte, J. A., Zergeroglu, A. M., & Demirel, H. A.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2012-07-01
- Volume
- 303
- Issue
- 1
- Pages
- E31-E39
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W1980638751
- Cited by
- 249
- References
- 17
- FWCI
- 5.46
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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