The DOI matches its Crossref record; 56 of the 57 references it cites were found in a registry or an index.
Interleukin 6 receptor antibody inhibits muscle atrophy and modulates proteolytic systems in interleukin 6 transgenic mice.
Open accessAbstract
The muscles of IL-6 transgenic mice suffer from atrophy. Experiments were carried out on these transgenic mice to elucidate activation of proteolytic systems in the gastrocnemius muscles and blockage of this activation by treatment with the anti-mouse IL-6 receptor (mIL-6R) antibody. Muscle atrophy observed in 16-wk-old transgenic mice was completely blocked by treatment with the mIL-6R antibody. In association with muscle atrophy, enzymatic activities and mRNA levels of cathepsins (B and L) and mRNA levels of ubiquitins (poly- and mono-ubiquitins) increased, whereas the mRNA level of muscle-specific calpain (calpain 3) decreased. All these changes were completely eliminated by treatment with the mIL-6R antibody. This IL-6 receptor antibody could, therefore, be effective against muscle wasting in sepsis and cancer cachexia, where IL-6 plays an important role.
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“the pilot study of Tsujinaka and colleagues showed that transgenic mice chronically overexpressing IL-6 exhibit a marked muscle atrophy [47]; however, the knockout of IL-6 was not sufficient to prevent sarcopenia in a sepsis mouse model [48].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [47]
In the citing paper
“However, it has also been shown that proinflammatory cytokines may inhibit muscle progenitor cell differentiation and that the reactive oxygen species that are produced by M1 cells (nitric oxide) can be cytotoxic if present in sufficient quantities, demonstrating the need for resolution of the proinflammatory response for muscle recovery to proceed beyond this initial stage [120–122].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [122]
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Cites
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[41] Cathepsin B, cathepsin H, and cathepsin L
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Mutations in the proteolytic enzyme calpain 3 cause limb-girdle muscular dystrophy type 2A
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Soluble interleukin-6 receptor triggers osteoclast formation by interleukin 6.
Tamura, T., Udagawa, N., Takahashi, N., Miyaura, C., Tanaka, S., Yamada, Y., Koishihara, Y., Ohsugi, Y., Kumaki, K., & Taga, T. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.24.11924 · Cited by 828
Self-citationEvidence for the involvement of interleukin 6 in experimental cancer cachexia.
Strassmann, G., Fong, M., Kenney, J. S., & Jacob, C. O. (1992) · Journal of Clinical Investigation · doi:10.1172/jci115767 · Cited by 660
IgG1 plasmacytosis in interleukin 6 transgenic mice
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Molecular cloning of a novel mammalian calcium-dependent protease distinct from both m- and μ-types
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Tisdale, M. J. (2009) · Physiological Reviews · doi:10.1152/physrev.00016.2008 · Cited by 1,216
Brown, B. N., Ratner, B. D., Goodman, S. B., Amar, S., & Badylak, S. F. (2012) · Biomaterials · doi:10.1016/j.biomaterials.2012.02.034 · Cited by 926
Stenvinkel, P., Ketteler, M., Johnson, R. J., Lindholm, B., Pecoits‐Filho, R., RIELLA, M. C., Heimbürger, O., Cederholm, T., & Girndt, M. (2005) · Kidney International · doi:10.1111/j.1523-1755.2005.00200.x · Cited by 952
“Moreover, IL-6 receptor antibody has been shown to inhibit muscle atrophy that occurs in IL-6 transgenic mice [70].”
BackgroundC-reactive protein predicts all-cause and cardiovascular mortality in hemodialysis patients
Yeun, J. Y., Levine, R. A., Mantadilok, V., & Kaysen, G. A. (2000) · American Journal of Kidney Diseases · doi:10.1016/s0272-6386(00)70200-9 · Cited by 885
Interleukin‐6 myokine signaling in skeletal muscle: a double‐edged sword?
Muñoz‐Cánoves, P., Scheele, C., Pedersen, B. K., & Serrano, A. L. (2013) · The FEBS Journal · doi:10.1111/febs.12338 · Cited by 774
Metadata
- Authors
- Tsujinaka, T., Fujita, J., Ebisui, C., Yano, M., Kominami, E., Suzuki, K., Tanaka, K., Katsume, A., Ohsugi, Y., Shiozaki, H., & Monden, M.
- Affiliations
- Osaka University Hospital (JP)
- The University of Osaka (JP)
- Juntendo University (JP)
- Institute for Quantitative Biosciences, The University of Tokyo (JP)
- Chugai Pharmaceutical Co., Ltd. (Japan) (JP)
- Venue
- Journal of Clinical Investigation
- Published
- 1996-01-01
- Volume
- 97
- Issue
- 1
- Pages
- 244-249
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC507086
- OpenAlex
- W2060757943
- Cited by
- 421
- References
- 57
- Citations by year
- 2026: 10 · 2025: 12 · 2024: 16 · 2023: 10 · 2022: 22 · 2021: 16 · 2020: 13 · 2019: 9 · 2018: 14 · 2017: 11 · 2016: 9 · 2015: 17 · 2014: 9 · 2013: 14 · 2012: 18
- FWCI
- 5.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology (medical) › Nutrition and Health in Aging
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Keywords
- interleukin-6, IL-6 receptor antibody, muscle atrophy, proteolytic system, cathepsin B, cathepsin L, ubiquitin, CAPN3, gastrocnemius, cancer cachexia, sepsis
- MeSH terms
- Animals, Antibodies, Monoclonal, Body Weight, Calpain, Cathepsin B, Cathepsins, Cysteine Endopeptidases, Humans, Mice, Inbred C57BL, Mice, Transgenic, Multienzyme Complexes, Muscular Atrophy, Organ Size, Endopeptidases, RNA, Messenger, Ubiquitins, Antigens, CD, Interleukin-6, Gene Expression, Rats, Wistar, Receptors, Interleukin, Muscle, Skeletal, Receptors, Interleukin-6, Proteasome Endopeptidase Complex, Mice, Rats, Cathepsin L
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