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Cited by 612Muscle Physiology and DisordersExercise and Physiological ResponsesMuscle metabolism and nutrition

The DOI matches its Crossref record; 59 of the 60 references it cites were found in a registry or an index.

IL-6-induced skeletal muscle atrophy

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Haddad, F., Zaldivar, F., Cooper, D. M., Adams, G. R.·2005·Journal of Applied Physiology
DOI 10.1152/japplphysiol.01026.2004
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Abstract

Chronic, low-level elevation of circulating interleukin (IL)-6 is observed in disease states as well as in many outwardly healthy elderly individuals. Increased plasma IL-6 is also observed after intense, prolonged exercise. In the context of skeletal muscle, IL-6 has variously been reported to regulate carbohydrate and lipid metabolism, increase satellite cell proliferation, or cause muscle wasting. In the present study, we used a rodent local infusion model to deliver modest levels of IL-6, comparable to that present after exercise or with chronic low-level inflammation in the elderly, directly into a single target muscle in vivo. The aim of this study was to examine the direct effects of IL-6 on skeletal muscle in the absence of systemic changes in this cytokine. Data included cellular and molecular markers of cytokine and growth factor signaling (phosphorylation and mRNA content) as well as measurements to detect muscle atrophy. IL-6 infusion resulted in muscle atrophy characterized by a preferential loss of myofibrillar protein (−17%). IL-6 induced a decrease in the phosphorylation of ribosomal S6 kinase (−60%) and STAT5 (−33%), whereas that of STAT3 was increased approximately twofold. The changes seen in the IL-6-infused muscles suggest alterations in the balance of growth factor-related signaling in favor of a more catabolic profile. This suggests that downregulation of growth factor-mediated intracellular signaling may be a mechanism contributing to the development of muscle atrophy induced by elevated IL-6.

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Crossref · 10.1152/japplphysiol.01026.2004

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Metadata

Authors
Haddad, F., Zaldivar, F., Cooper, D. M., & Adams, G. R.
Affiliations
University of California, Irvine (US)
ORCID
Haddad, F.
Venue
Journal of Applied Physiology
Publisher
American Physiological Society
Published
2005-03
Volume
98
Issue
3
Pages
911-917
ISSN
  • 0161-7567 (ISSN-L)
  • 8750-7587
  • 1522-1601
DOI
10.1152/japplphysiol.01026.2004
OpenAlex
W2121311831
Cited by
612
References
60
Citations by year
2026: 27 · 2025: 34 · 2024: 39 · 2023: 37 · 2022: 43 · 2021: 34 · 2020: 37 · 2019: 35 · 2018: 40 · 2017: 17 · 2016: 28 · 2015: 43 · 2014: 20 · 2013: 32 · 2012: 26
FWCI
4.26
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Journal of Applied Physiology (publishedVersion)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion, cc-by)
Funders
  • National Institutes of Health (5r01ar045594-05)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-45594)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
  • Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
Keywords
interleukin-6, skeletal muscle atrophy, myofibrillar protein degradation, RSK, STAT5, STAT3, cytokine signaling, muscle atrophy, muscle catabolism, satellite cells, aging, physical activity
MeSH terms
Animals, Female, Muscle Proteins, Muscular Atrophy, Signal Transduction, Interleukin-6, Rats, Sprague-Dawley, Rats

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