The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
Glucocorticoid-induced skeletal muscle atrophy is associated with upregulation of myostatin gene expression
Abstract
The mechanisms by which excessive glucocorticoids cause muscular atrophy remain unclear. We previously demonstrated that dexamethasone increases the expression of myostatin, a negative regulator of skeletal muscle mass, in vitro. In the present study, we tested the hypothesis that dexamethasone-induced muscle loss is associated with increased myostatin expression in vivo. Daily administration (60, 600, 1,200 μg/kg body wt) of dexamethasone for 5 days resulted in rapid, dose-dependent loss of body weight (-4.0, -13.4, -17.2%, respectively, P < 0.05 for each comparison), and muscle atrophy (6.3, 15.0, 16.6% below controls, respectively). These changes were associated with dose-dependent, marked induction of intramuscular myostatin mRNA (66.3, 450, 527.6% increase above controls, P < 0.05 for each comparison) and protein expression (0.0, 260.5, 318.4% increase above controls, P < 0.05). We found that the effect of dexamethasone on body weight and muscle loss and upregulation of intramuscular myostatin expression was time dependent. When dexamethasone treatment (600 μg · kg-1 · day-1) was extended from 5 to 10 days, the rate of body weight loss was markedly reduced to ∼2% within this extended period. The concentrations of intramuscular myosin heavy chain type II in dexamethasone-treated rats were significantly lower (-43% after 5-day treatment, -14% after 10-day treatment) than their respective corresponding controls. The intramuscular myostatin concentration in rats treated with dexamethasone for 10 days returned to basal level. Concurrent treatment with RU-486 blocked dexamethasone-induced myostatin expression and significantly attenuated body loss and muscle atrophy. We propose that dexamethasone-induced muscle loss is mediated, at least in part, by the upregulation of myostatin expression through a glucocorticoid receptor-mediated pathway.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Double muscling in cattle due to mutations in the myostatin gene
McPherron, A. C., & Lee, S.-J. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.23.12457 · Cited by 2,039
Regulation of myostatin activity and muscle growth
Lee, S.-J., & McPherron, A. C. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.151270098 · Cited by 1,616
A deletion in the bovine myostatin gene causes the double–muscled phenotype in cattle
Grobet, L., Royo Martin, L. J., Poncelet, D., Pirottin, D., Brouwers, B., Riquet, J., Schoeberlein, A., Dunner, S., Ménissier, F., Massabanda, J., et al. (1997) · Nature Genetics · doi:10.1038/ng0997-71 · Cited by 1,556
Mutations in myostatin ( GDF8 ) in Double-Muscled Belgian Blue and Piedmontese Cattle
Kambadur, R., Sharma, M., Smith, T. P. L., & Bass, J. J. (1997) · Genome Research · doi:10.1101/gr.7.9.910 · Cited by 1,204
Mechanisms of Muscle Wasting — The Role of the Ubiquitin–Proteasome Pathway
Mitch, W. E., & Goldberg, A. L. (1996) · New England Journal of Medicine · doi:10.1056/nejm199612193352507 · Cited by 1,166
Myostatin, a Negative Regulator of Muscle Growth, Functions by Inhibiting Myoblast Proliferation
Thomas, M., Langley, B., Berry, C., Sharma, M., Kirk, S., Bass, J., & Kambadur, R. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.m004356200 · Cited by 1,014
Electrophoretic separation of rat skeletal muscle myosin heavy-chain isoforms
Talmadge, R. J., & Roy, R. R. (1993) · Journal of Applied Physiology · doi:10.1152/jappl.1993.75.5.2337 · Cited by 803
Gonzalez-Cadavid, N. F., Taylor, W. E., Yarasheski, K., Sinha-Hikim, I., Ma, K., Ezzat, S., Shen, R., Lalani, R., Asa, S., Mamita, M., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.25.14938 · Cited by 571
Self-citationControl of muscle development by dueling HATs and HDACs
McKinsey, T. A., Zhang, C. L., & Olson, E. N. (2001) · Current Opinion in Genetics & Development · doi:10.1016/s0959-437x(00)00224-0 · Cited by 414
Myostatin inhibits cell proliferation and protein synthesis in C2C12 muscle cells
Taylor, W. E., Bhasin, S., Artaza, J., Byhower, F., Azam, M., Willard, D. H., Kull, F. C., & Gonzalez-Cadavid, N. (2001) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.2001.280.2.e221 · Cited by 410
Self-citation
Cited by
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
REGULATION OF MUSCLE MASS BY MYOSTATIN
Lee, S.-J. (2004) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev.cellbio.20.012103.135836 · Cited by 819
Glucocorticoid-Induced Skeletal Muscle Atrophy
Schakman, O., Kalista, S., Barbé, C., Loumaye, A., & Thissen, J. P. (2013) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2013.05.036 · Cited by 705
Glucocorticoids, metabolism and metabolic diseases
Vegiopoulos, A., & Herzig, S. (2007) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2007.05.015 · Cited by 535
Mechanisms of glucocorticoid-induced myopathy
Schakman, O., Gilson, H., & Thissen, J. P. (2008) · Journal of Endocrinology · doi:10.1677/joe-07-0606 · Cited by 521
Metadata
- Authors
- Ma, K., Mallidis, C., Bhasin, S., Mahabadi, V., Artaza, J., Gonzalez-Cadavid, N., Arias, J., & Salehian, B.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2003-08
- Volume
- 285
- Issue
- 2
- Pages
- E363-E371
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2116082328
- Cited by
- 414
- References
- 44
- FWCI
- 5.25
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Glucocorticoid-induced skeletal muscle atrophy is associated with upregulation of myostatin gene expression. https://app.cochat.ai/papers/10.1152/ajpendo.00487.2002
- The paper
- Ma, K., Mallidis, C., Bhasin, S., Mahabadi, V., Artaza, J., Gonzalez-Cadavid, N., Arias, J., & Salehian, B. (2003). Glucocorticoid-induced skeletal muscle atrophy is associated with upregulation of myostatin gene expression. American Journal of Physiology-Endocrinology and Metabolism. https://doi.org/10.1152/ajpendo.00487.2002
Data sources
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).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
