The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Doxorubicin acts via mitochondrial ROS to stimulate catabolism in C2C12 myotubes
Open accessAbstract
Doxorubicin, a commonly prescribed chemotherapeutic agent, causes skeletal muscle wasting in cancer patients undergoing treatment and increases mitochondrial reactive oxygen species (ROS) production. ROS stimulate protein degradation in muscle by activating proteolytic systems that include caspase-3 and the ubiquitin-proteasome pathway. We hypothesized that doxorubicin causes skeletal muscle catabolism through ROS, causing upregulation of E3 ubiquitin ligases and caspase-3. We tested this hypothesis by exposing differentiated C2C12 myotubes to doxorubicin (0.2 μM). Doxorubicin decreased myotube width 48 h following exposure, along with a 40–50% reduction in myosin and sarcomeric actin. Cytosolic oxidant activity was elevated in myotubes 2 h following doxorubicin exposure. This increase in oxidants was followed by an increase in the E3 ubiquitin ligase atrogin-1/muscle atrophy F-box (MAFbx) and caspase-3. Treating myotubes with SS31 (opposes mitochondrial ROS) inhibited expression of ROS-sensitive atrogin-1/MAFbx and protected against doxorubicin-stimulated catabolism. These findings suggest doxorubicin acts via mitochondrial ROS to stimulate myotube atrophy.
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Cites
Mitochondrial formation of reactive oxygen species
Turrens, J. F. (2003) · The Journal of Physiology · doi:10.1113/jphysiol.2003.049478 · Cited by 5,084
Anderson, E. J., Lustig, M. E., Boyle, K. E., Woodlief, T. L., Kane, D. A., Lin, C.-T., Price, J. W., Kang, L., Rabinovitch, P. S., Szeto, H. H., et al. (2009) · Journal of Clinical Investigation · doi:10.1172/jci37048 · Cited by 1,253
The Molecular Basis of Skeletal Muscle Atrophy
Jackman, R. W., & Kandarian, S. C. (2004) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00579.2003 · Cited by 1,008 · cited 1×
“systems including caspase-3 and the ubiquitin-proteasome pathway (3, 4, 21).”
BackgroundZhao, K., Zhao, G.-M., Wu, D., Soong, Y., Birk, A. V., Schiller, P. W., & Szeto, H. H. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m402999200 · Cited by 782
Oxidative Stress, Chronic Disease, and Muscle Wasting
Moylan, J. S., & Reid, M. B. (2007) · Muscle & Nerve · doi:10.1002/mus.20743 · Cited by 416
Self-citationMechanisms of disuse muscle atrophy: role of oxidative stress
Powers, S. K., Kavazis, A. N., & DeRuisseau, K. C. (2005) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00469.2004 · Cited by 368
Patterns of gene expression in atrophying skeletal muscles: response to food deprivation
Jagoe, R. T., Lecker, S. H., Gomes, M., & Goldberg, A. L. (2002) · The FASEB Journal · doi:10.1096/fj.02-0312com · Cited by 344
Cited by
Szeto, H. H. (2014) · British Journal of Pharmacology · doi:10.1111/bph.12461 · Cited by 548
Mitochondrial quality control and muscle mass maintenance.
Romanello, V., & Sandri, M. (2016) · Frontiers in Physiology · doi:10.3389/fphys.2015.00422 · Cited by 434
Gorini, S., De Angelis, A., Berrino, L., Malara, N., Rosano, G., & Ferraro, E. (2018) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2018/7582730 · Cited by 325
The Role of Oxidative Stress in Skeletal Muscle Myogenesis and Muscle Disease
Lian, D., Chen, M.-M., Wu, H., Deng, S., & Hu, X. (2022) · Antioxidants · doi:10.3390/antiox11040755 · Cited by 232
Park, B.-S., Henning, P. C., Grant, S. C., Lee, W. J., Lee, S.-R., Arjmandi, B. H., & Kim, J.-S. (2013) · Metabolism · doi:10.1016/j.metabol.2013.06.005 · Cited by 49
Metadata
- Authors
- Gilliam, L. A. A., Moylan, J. S., Patterson, E. W., Smith, J. D., Wilson, A. S., Rabbani, Z., & Reid, M. B.
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2012-01
- Volume
- 302
- Issue
- 1
- Pages
- C195-C202
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- OpenAlex
- W2146958737
- Cited by
- 161
- References
- 7
- FWCI
- 2.23
- Type
- journal article
- Language
- en
- Open access
- green
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- Gilliam, L. A. A., Moylan, J. S., Patterson, E. W., Smith, J. D., Wilson, A. S., Rabbani, Z., & Reid, M. B. (2012). Doxorubicin acts via mitochondrial ROS to stimulate catabolism in C2C12 myotubes. American Journal of Physiology-Cell Physiology. https://doi.org/10.1152/ajpcell.00217.2011
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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